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Critical Reviews in Food Science and Nutrition Volume 63, 2023 - Issue 24
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Review Articles

Involvement of microRNA modifications in anticancer effects of major polyphenols from green tea, coffee, wine, and curry

Tomokazu Ohishia Institute of Microbial Chemistry (BIKAKEN), Numazu, Microbial Chemistry Research Foundation, Shizuoka, JapanCorrespondenceohishit@bikaken.or.jp
ORCID Iconhttps://orcid.org/0000-0002-9039-4474
ORCID Icon,
Sumio Hayakawab Department of Biochemistry and Molecular Biology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan
&
Noriyuki Miyoshic Laboratory of Biochemistry, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka, JapanCorrespondencemiyoshin@u-shizuoka-ken.ac.jp
ORCID Iconhttps://orcid.org/0000-0002-4233-4282
ORCID Icon
Pages 7148-7179 | Published online: 15 Mar 2022

Abstract

Epidemiological studies have shown that consumption of green tea, coffee, wine, and curry may contribute to a reduced risk of various cancers. However, there are some cancer site-specific differences in their effects; for example, the consumption of tea or wine may reduce bladder cancer risk, whereas coffee consumption may increase the risk. Animal and cell-based experiments have been used to elucidate the anticancer mechanisms of these compounds, with reactive oxygen species (ROS)-based mechanisms emerging as likely candidates. Chlorogenic acid (CGA), curcumin (CUR), epigallocatechin gallate (EGCG), and resveratrol (RSV) can act as antioxidants that activate AMP-activated protein kinase (AMPK) to downregulate ROS, and as prooxidants to generate ROS, leading to the downregulation of NF-κB. Polyphenols can modulate miRNA (miR) expression, with these dietary polyphenols shown to downregulate tumor-promoting miR-21. CUR, EGCG, and RSV can upregulate tumor-suppressing miR-16, 34a, 145, and 200c, but downregulate tumor-promoting miR-25a. CGA, EGCG, and RSV downregulate tumor-suppressing miR-20a, 93, and 106b. The effects of miRs may combine with ROS-mediated pathways, enhancing the anticancer effects of these polyphenols. More precise analysis is needed to determine how the different modulations of miRs by polyphenols relate to the cancer site-specific differences found in epidemiological studies related to the consumption of foods containing these polyphenols.

Introduction

Plant polyphenols are found in various foods, such as tea, apples, onions, berries, citrus fruits, plums, broccoli, cocoa, and coffee (Tanabe et al. Citation2017). These polyphenols include flavanols such as tea catechins, apple epicatechin, cocoa procyanidins; flavonols such as onion quercetin; flavanones such as citrus fruit hesperidin; hydrocinnamic acids such as coffee chlorogenic acid (CGA); anthocyanins such as berry cyanidins, curcuminoids such as turmeric curcumin (CUR); and resveratrol (RSV) (). Recent studies have identified the health-beneficial effects of these polyphenols on a variety of diseases, including cancer, obesity, and neurodegenerative diseases. Our previous review articles examined the effect of commonly consumed dietary polyphenols, CGA, CUR, and (−)-epigallocatechin-3-gallate (EGCG), the most abundant green tea catechin, and RSV on cancer, obesity, and neurodegenerative diseases () (Fukutomi et al. Citation2021; Hayakawa et al. Citation2020; Ohishi et al. Citation2021). Observational and experimental epidemiology have provided evidence that the consumption of coffee, green tea, wine, and curry confer protective health benefits against cancer, although contrasting viewpoints have also been reported (Fukutomi et al. Citation2021; Hayakawa et al. Citation2020; Ohishi et al. Citation2021; Tanabe et al. Citation2017).

Figure 1. Chemical structures of chlorogenic acid (CGA), curcumin (CUR), epigallocatechin gallate (EGCG), and resveratrol (RSV).

Figure 1. Chemical structures of chlorogenic acid (CGA), curcumin (CUR), epigallocatechin gallate (EGCG), and resveratrol (RSV).

The results of many cell-based and preclinical studies have supported these effects and provided the mechanistic bases of action (Fukutomi et al. Citation2021; Hayakawa et al. Citation2020; Ohishi et al. Citation2021; Tanabe et al. Citation2017). Among the various mechanisms associated with these polyphenols, mechanisms involving reactive oxygen species (ROS) appear to be the most likely candidates (Hayakawa et al. Citation2020). In addition, there is an increasing number of studies that investigate the involvement of epigenetic modifications by these polyphenols in cancer and other diseases (Arshad and Ahmad Citation2021). Epigenetic modifications include posttranslational changes in histones and DNA, such as methylation and acetylation, as well as the dysregulation of noncoding RNAs (ncRNAs) such as miRNAs (miRs) and long ncRNAs, where miRs are defined as small single-stranded molecules (ca. 20 to 25 nucleotides) and long ncRNAs as RNA molecules larger than 200 nucleotides (Hayakawa et al. Citation2020). These ncRNAs can regulate gene expression at the transcriptional and posttranscriptional levels and are thought to be involved in the mechanisms of health-beneficial effects exerted by these polyphenols in diseases, including cancer (Hayakawa et al. Citation2020; Sakamoto et al. Citation2017).

In this review, we discuss the up-to-date evidence from human studies, which supports the anticancer effects of the consumption of coffee, green tea, red wine, and curry, and discuss the mechanistic aspects of the actions of their main polyphenols based on the results of cell-based and animal experiments, with a focus on their regulation of miRs.

Coffee/CGA

Human studies on anticancer effects of coffee

Although some earlier epidemiological studies have shown that coffee consumption had no association, or even an unfavorable association, with the risk of bladder, breast, colorectal, lung, pancreatic, and prostate cancers (PCa) (Hayakawa et al. Citation2020; Wierzejska Citation2015), several studies have supported the anticancer effects of coffee. For example, Tran et al. (Citation2019) reported that a large number of epidemiological and experimental studies showed the anticancer effects of coffee on liver and endometrial cancers. A meta-analysis of observational studies on 26 different cancers, including 364,749 cases of cancer, found an inverse association of coffee with endometrial cancer, liver cancer, melanoma, oral cancer, and oral/pharyngeal cancer (L. G. Zhao et al. Citation2020). In a study conducted by Gapstur et al. (Citation2017) on nonsmokers, an increase in coffee intake of two cups per day was inversely associated with death from colorectal cancer (CRC) (hazard ratio (HR) = 0.97; 95% confidence interval (CI) = 0.95–0.99), liver cancer (HR = 0.92; CI = 0.88–0.96), and breast cancer (BCa) (HR = 0.97; CI = 0.94–0.99), although a positive association was found with esophageal cancer-related death (HR = 1.07; CI = 1.02–1.12).

More recent studies have also shown the following anticancer effects of coffee. In a systematic review of 22 case–control studies and a meta-analysis of 20 studies, a significant association was not found between the risk of ovarian cancer and total coffee intake or caffeinated coffee intake. However, the further combined analysis of five studies showed an inverse significant association between decaffeinated coffee intake and ovarian cancer risk (odds ratio (OR) = 0.72; CI 0.58–0.90) (Shafiei et al. Citation2019). Therefore, caffeine may be not involved in the effect of coffee against this cancer (Shafiei et al. Citation2019).

A retrospective case–control study of 17,093 patients with synchronous CRC showed that compared with patients without daily coffee consumption, daily coffee consumption resulted in significantly higher 5-year overall survival rate in stages I (93.0% vs. 86.4%), II (87.1% vs. 77.2%), III (71.5% vs. 61.9%), and IV (18.0% vs. 13.0%), suggesting its role for protecting against synchronous CRC (Kuo et al. Citation2019).

A meta-analysis of six case-control studies and two cohort studies revealed that high coffee intake was associated with a reduced risk of colorectal adenoma (Y. Wang et al. Citation2020). The dose-response meta-analysis indicated that the estimated total OR for increasing coffee consumption by 150 mL/day (about one cup) was 0.91 (CI = 0.87–0.95).

Similarly, a meta-analysis showed that the occurrence of thyroid cancer (TCa) was reduced by 5% with an increase of one cup per day in coffee consumption with summary adjusted relative risk (RR) = 0.95; CI = 0.91–0.99 (Shao et al. Citation2020).

A prospective cohort study on 1,171 patients with previously untreated locally advanced or metastatic CRC found an inverse association between coffee consumption and the risk of cancer progression (HR for 1 cup/day increment = 0.95; CI = 0.91–1.00) and death (HR for 1 cup/day increment = 0.93; CI = 0.89–0.98), suggesting that coffee may protect from disease progression and death in advanced or metastatic CRC (Mackintosh et al. Citation2020). Significant associations were also found for both caffeinated and decaffeinated coffee, indicating that caffeine was not likely to contribute to these effects.

In a systematic review and dose-response meta-analysis, Pranata et al. (Citation2022) found that higher coffee consumption was associated with a lower risk of glioma, but the trend was not statistically significant. When the case-control studies were excluded, higher coffee consumption was found to be significantly associated with a lower risk of glioma. The dose-response meta-analysis indicated that one cup of coffee per day decreased the risk of glioma by 3% (RR = 0.97; CI = 0.94–0.99), showing an inverse association between coffee and the risk of glioma.

A systematic review of 45 studies that included more than 3,323,288 participants demonstrated that coffee and tea consumption was not associated with a reduction in the overall BCa risk in postmenopausal women, but suggested that it was associated with a lower risk of estrogen receptor-negative BCa (Wang et al. Citation2021). These authors recommended daily doses of 2–3 cups/day of coffee containing a high concentration of caffeine, particularly in postmenopausal women.

An evaluation of findings from Mendelian randomization studies and the corresponding observational studies showed an association between high coffee consumption and a low risk of endometrial cancer and melanoma in observational studies (Nordestgaard Citation2021).

In contrast, high coffee consumption was associated with a high risk of lung cancer in observational studies and with a high risk of CRC in Mendelian randomization studies (Nordestgaard Citation2021). Similarly, several studies did not show the anticancer effects of coffee. The consumption of a higher coffee intake may be associated with an increased risk of childhood acute lymphocytic leukemia, bladder cancer, and possibly lung cancer (L. G. Zhao et al. Citation2020). A recent pooled analysis of 501,604 participants from 12 cohort studies on BCa showed that after adjustment for confounders, high coffee consumption (>500 mL/day, equivalent to >4 cups/day) is associated with a higher risk among male smokers (current smokers: HR = 1.75; CI = 1.27–2.42; former smokers: HR = 1.44; CI = 1.12–1.85) compared with never consumers. These authors found inconsistent results between sexes and the absence of an association in never-smokers, which suggested that the association found among male smokers may be caused by residual confounding of smoking behavior (Yu et al. Citation2020). Other studies have also failed to show a significant inverse association between coffee intake and TCa (Zamora-Ros et al. Citation2019), lung cancer, BCa, CRC, and PCa, or overall cancer (Rosato et al. Citation2021; Schmit et al. Citation2020). Even a positive association was found between an intake of five or more cups/day in gastric cardia cancer (Martimianaki et al. Citation2021).

These conflicting results may have come from the recall bias and confounding factors, such as tobacco smoking, coffee type, brewing method, differences in ingredients, the presence or absence of added sugar and cream, and the patient’s genetic background (Hayakawa et al. Citation2020; Shahinfar et al. Citation2021).

Curry/CUR

Human studies on anticancer effects of curry/CUR

A number of phase I trials on the anticancer effects of CUR have been conducted, showed the safety, and recommended dose of CUR and its derivatives, such as THERACURMIN, curcuRougeTM, and CUR phytosome (Meriva) (Bayet-Robert et al. Citation2010; Kanai Citation2014; Kishimoto et al. Citation2021).

In phase I/II clinical trials, the favorable effects of CUR were observed in several types of cancer. In a clinical study studying 39 and 43 patients in the CUR and placebo groups, respectively, Choi et al. (Citation2019) found that PCa-specific antigen (PSA) elevation was suppressed by oral CUR intake (1,440 mg/day) for 6 months.

A phase IIB trial conducted by Kuriakose et al. (Citation2016) evaluated the efficacy of CUR on oral leukoplakia, a potentially malignant lesion of the oral cavity. By using the response criteria of disappearance of the lesion [complete response (CR)] and 50% or greater decrease in the sum of diameters of all lesions [partial response (PR)], 75 of 105 patients in the CUR group and 62 of 108 placebo patients had a clinical response (CR + PR) with a statistical difference at P = 0.03. When the clinical response was combined with the histologic response evaluated for histologic complete reversal of dysplasia/hyperplasia to the normal epithelium and the regression degree of dysplasia, the difference between the CUR and placebo groups was also statistically significant. CUR appears to be clinically effective in treating oral leukoplakia and may have a chemopreventive potential in oral cancer.

In a nonrandomized, open-label clinical trial in 44 smokers with ≥8 aberrant crypt foci (ACF), a 40% reduction in ACF number was found in the 4 g dose group (P < 0.005), but not in the 2 g group (Carroll et al. Citation2011).

In patients with pancreatic cancer resistant to gemcitabine-based chemotherapy (Kanai et al. Citation2011), the inclusion of an oral dose of CUR 8 g/day resulted in a median survival time of 5.4 (CI = 3.6–7.4) months and a 1-year survival rate of 19% (CI = 4.4%–41.4%). These results appear promising in view of the poor prognosis of patients with pancreatic cancer with resistance to gemcitabine-based chemotherapy.

Ryan et al. (Citation2013) found that oral CUR administration during radiotherapy reduced the severity of radiation dermatitis in patients with breast cancer in a randomized controlled trial (RCT) where randomized patients took 6.0 g/day of CUR or placebo orally.

In a clinical study on patients with CRC, CUR resulted in favorable effects, such as decreased serum tumor necrosis factor (TNF)-α levels, increased apoptotic tumor cells, enhanced expression of the p53 molecule in tumor tissue, and modulation of the tumor cell apoptosis pathway, suggesting that CUR can improve the general health of these patients by increasing p53 expression in tumor cells and enhancing tumor cell apoptosis (He et al. Citation2011).

A pilot study using the curcuminoid preparation Meriva by Ledda et al. (Citation2012) found that the quality of life was significantly better in the CUR group who received Meriva in addition to the standard treatment. Significant decreases in clinical and subclinical episodes of urinary infections and urinary block were also observed.

In a clinical trial of 80 patients with solid tumors treated with standard chemotherapy, received Meriva (180 mg/day; n = 40) or placebo (n = 40) for a period of 8 weeks (Panahi et al. Citation2014). The Meriva group showed a significantly greater improvement in quality of life compared with the placebo group. Significant reductions were also found in biomarkers, such as TNF-α, transforming growth factor (TGF)-β, C-reactive protein, and Monocyte chemoattractant protein-1 in placebo than in the Meriva group, whereas reduction in the serum interleukin-8 (IL-8) level was less than placebo.

Some of the recent clinical trials on CUR as a therapeutic agent in various cancers (https://clinicaltrials.gov/) have confirmed the effectiveness of CUR combination therapy in BCa, CRC, PCa, and chronic myeloid leukemia, and less significant effectiveness in pancreatic cancer (Kong et al. Citation2021; Mari et al. Citation2021). The anticancer activity of CUR against several cancers, for example, gastrointestinal, head and neck, brain, pancreatic, colorectal, breast, and prostate cancers has also been reported (Kabir et al. Citation2021).

Radiotherapy may cause oral mucositis, which is a severe nonhematological complication in patients with head and neck cancer. A pilot RCT using 0.1% CUR nanoparticles and 0.15% benzydamine mouthwash showed that the use of CUR mouthwash was able to significantly delay the onset of radiotherapy-induced oral mucositis (Shah et al. Citation2020).

In contrast, there are many studies reporting no or adverse effects of CUR on cancers. For example, a recent systematic review of seven papers led Shafei et al. (Citation2021) to the conclusion that there were no studies showing improvement or regression in colon cancer. Although two studies indicated that CUR was effective at the molecular and histological levels, other studies found unfavorable effects, including disease progression, a fatality, and liver metastasis. Passildas-Jahanmohan et al. (Citation2021) reported that their phase II study on metastatic castration-resistant PCa found that oral administration of CUR (6 g/day for 7 days) combined with docetaxel did not improve either progression-free survival or overall survival. The authors claimed that the result may have arisen from the poor bioavailability of CUR. Future human studies are required to confirm the anticancer effects of CUR.

Tea/EGCG

Human studies on anticancer effects of green tea/EGCG

Our previous review demonstrated the anticancer effects of green tea/EGCG (Hayakawa et al. Citation2020). A survey of epidemiological studies conducted by X. Y. Xu et al. (Citation2020) found that 5 of total 11 studies showed the favorable effects of tea consumption. Many human studies published from 2019 to April 2020 also showed the anticancer effects of green tea (Hayakawa et al. Citation2020). For example, a population-based prospective cohort study of 13,957 men and 16,374 women found the multiple-adjusted risk of colon cancer (RR = 0.78; CI = 0.49–1.22) of men consuming ≥4 cups of green tea daily was lower compared to the <1 cup consumers (K. Wada et al. Citation2019).

Polyphenon E, or sinecatechins, is a standardized catechin preparation of green tea extract with approval of the United States Food and Drug Administration in 2006 for the topical treatment of genital warts caused by human papilloma viruses (HPV) (Hayakawa et al. Citation2020). Several clinical studies have shown its efficacy to cause significantly higher rates of complete clearance of baseline and new warts compared with controls, with very low recurrence rates (Tzellos et al. Citation2011). In a clinical trial, 51 patients with HPV-infected cervical lesions treated with Polyphenon E ointment or capsules or both, showed an overall response rate of 69% compared with that of 10% in the untreated groups (Ahn et al. Citation2003). The results of another phase II trial in 42 patients with asymptomatic, chronic lymphocytic leukemia, Polyphenon E caused a sustained reduction of ≥20% of the absolute lymphocyte count in 31% of patients and a ≥ 50% reduction in palpable lymphadenopathy in 69% of patients (Shanafelt et al. Citation2013), suggesting the anticancer effects of green tea catechin extracts.

In a meta-analysis of eight cohort studies and five case–control studies, Gianfredi et al. (Citation2018) reported an inverse relationship between green tea intake and BCa risk with an OR of 0.85 (CI = 0.80–0.92), showing a potential protective effect of green tea on BCa, especially for BCa recurrence.

In the examination of a total of 1,551 Chinese patients with BCa, progression-free survival was found to be better among women who regularly drank any kind of tea (mainly green tea) compared with nontea drinkers (HR = 0.52; CI = 0.29–0.91) (Zhang et al. Citation2019). An intake of ≥7 times/week was significantly associated with better prognosis (HR = 0.30; CI = 0.11–0.84).

A survey by Grammatikopoulou et al. (Citation2020) on patients with PCa found a decrease in the PSA levels in three out of six RCTs studying the effect of green tea and/or green tea catechins (GTC), with no effects found in the other studies.

The results of a dose-response meta-analysis indicated that higher green tea consumption was linearly associated with a reduced risk of PCa with the consumption of more than seven cups per day (Guo et al. Citation2017). When the highest and lowest categories were compared, each increase in green tea consumption of one cup per day of green tea showed an insignificant reduction in PCa.

A meta-analysis of four studies containing a pooled population of 223 patients with PCa showed a significant reduction in cancer risk in the GTC group (risk ratio = 0.41; CI: 0.19–0.86), suggesting that GTC may have a significant anticancer effect on carriers of early neoplastic lesions in the prostate (Perletti et al. Citation2019).

Thus, although many studies in humans have found anticancer effects of green tea consumption, there are still several conflicting results. For example, three studies found that green tea consumption was not associated with a reduction in the risk of cervical, liver, and stomach cancers (Hayakawa et al. Citation2020), and the intake of double-brewed green tea, an EGCG-enriched tea drink, appeared not to be a promising maintenance of intervention in women with advanced stage ovarian cancer after standard treatment (Trudel et al. Citation2013). A recent analysis by Li et al. (Citation2019) found that the daily consumption of tea leaves of more than 4.0 g/day resulting in an elevated risk of all cancers (HR = 1.13; CI = 1.07–1.20), lung cancer (HR = 1.31; CI = 1.17–1.46), and stomach cancer (HR = 1.18; CI = 1.02–1.37), compared with less-than-weekly consumption. No association was found for CRC, liver cancer, BCa, and cervix uteri cancer.

The results of more recent comprehensive analysis showed that prospective studies have provided little evidence to indicate the inverse association of tea consumption with cancer risk (L. G. Zhao et al. Citation2021). These results provided weak evidence of favorable effects only on lymphoid neoplasm by the consumption of green tea. Total tea consumption may have benefits on glioma, bladder cancer, and gastric and esophageal cancer.

These inconsistent results may reflect various confounding factors, including tobacco smoking, genetic differences, hormonal activities, and microbiota (Hayakawa et al. Citation2020; Li et al. Citation2019; L. G. Zhao et al. Citation2021).

Wine/RSV

Human studies on anticancer effects of wine/RSV

In 1988, alcoholic beverages were classified as a group 1 carcinogen, the most severe classification, by the International Agency for Research on Cancer (International Agency for Research on Cancer and IARC Working Group on the Evaluation of Carcinogenic Risks to Humans Citation1988). A meta-analysis conducted by Bagnardi et al. (Citation2001), which included a total of 235 studies, found that alcohol intake resulted in strong trends in the increased risk for cancers of the oral cavity, pharynx, esophagus, and larynx. Less strong direct relations were observed for cancers of the stomach, colon, rectum, liver, breast, and ovary.

Rumgay et al. (Citation2021) also documented a causal relationship to alcohol consumption for cancers of the oral cavity, pharynx, larynx, esophagus, and liver, and subsequently for CRC, female BCa, and pancreatic cancer. It is notable that alcohol consumption may have different burdens depending on the cancer type, as esophagus, liver, and breast cancers are more related to alcohol consumption than other cancer types (Rumgay et al. Citation2021).

Other studies have also failed to show the anticancer effects of wine consumption. A prospective cohort study on 50–76-year-old residents in Washington state demonstrated no clear association between lung cancer and the consumption of beer, red wine, white wine, or liquor at ≥1 drink/day (Chao et al. Citation2011). Although a combined alcoholic beverage intake of up to ≥3 drinks/day was not associated with elevated lung cancer risk, an elevated risk for squamous cell carcinoma was found with the consumption of ≥3 drinks/day.

Barra et al. (Citation1990) and Bosetti et al. (Citation2000) found greater risks of oral, pharyngeal, and esophageal cancer in drinkers of wine compared with other alcoholic beverages after appropriate adjustments.

Hong et al. (Citation2020) conducted a meta-analysis of cohort studies on the association between the consumption of different types of alcohol and the risks for aggressive and nonaggressive types of PCa. The results indicated that wine was not associated with the risk of nonaggressive PCa, although higher doses of wine were significantly associated with a higher risk compared to nondrinking. It is interesting to note that the risks were reduced at lower doses of beer (RR = 0.85; CI = 0.79–0.92 at 14 g/day and RR = 0.79; CI = 0.70–0.90 at 28 g/day) and total alcohol consumption was not associated with both types of PCa.

When combinations of a micronized oral formulation of RSV and drugs such as bortezomib were used, patients with relapsed or refractory multiple myeloma manifested an unacceptable safety profile and minimal efficacy, showing the risks of novel drug development in such populations (Popat et al. Citation2013).

In contrast, several studies have demonstrated that wine may have anticancer effects. A case–control study by Kontou et al. (Citation2012) found that red wine intake was associated with reduced risk of CRC, which was significant in men (OR = 0.47; CI, 0.23–0.96) but not in women (OR = 0.54; CI = 0.23–1.30).

In a prospective cohort study of 24,244 participants, Park et al. (Citation2009) examined whether the consumption of any specific type of alcoholic beverage was related to overall or site-specific CRC risk. No significant associations were found between the consumption of specific alcoholic beverages (beer, sherry, or spirits) and CRC risk when compared with nondrinkers after adjustment, but inverse associations were found with the daily consumption of ≥1 unit of wine (HR = 0.61; CI = 0.40–0.94).

In a clinical study of Patel et al. (Citation2010), 20 patients with CRC received daily doses of RSV at 0.5 or 1.0 g for 8 days. RSV was found to be well tolerated and to decrease the tumor volume by 5%, as measured in biopsy tissue samples. Moreover, RSV caused a reduction in tumor cell proliferation by 5% (P = 0.05), as measured by the histological detection of Ki-67. These findings suggest that RSV may contribute to the reducing effect of wine on the CRC risk (Farinetti et al. Citation2017).

Brown et al. (Citation2010) conducted a clinical study in which 40 healthy volunteers were orally administered RSV at 0.5, 1.0, 2.5, or 5.0 g daily for 29 days. Although mild to moderate gastrointestinal symptoms were detected with 2.5 and 5 g doses, RSV reduced the levels of plasma insulin-like growth factor-I (IGF-I) and insulin-like growth factor-binding protein 3 in all volunteers compared with the values without an RSV dose, with the most marked decrease at the 2.5 g dose. As high levels of IGF-I have been causally associated with the risk of several cancers (Sandhu et al. Citation2002), this finding is suggestive of the anticancer effect of RSV.

In an RCT, 39 adult women at increased risk of BCa received placebo, 5 or 50 mg RSV twice daily for 12 weeks (Zhu et al. Citation2012). The methylation of Ras-association domain family (RASSF)-1α, a tumor suppressor gene, was significantly decreased as the levels of serum RSV increased and the change was directly related to that in prostaglandin E2, which has a tumor promotional property, suggesting a possible beneficial role against cancer.

By reviewing a number of clinical studies, Ramirez-Garza et al. (Citation2018) concluded that the intake of RSV was safe at a dose of up to 5 g, although various adverse effects may be experienced. Although RSV can have favorable effects, such as improved antioxidant capacity and modulated neuroinflammation, deleterious effects should also be considered. Conflicting results may be due to the effects of the dose ingested, the gut microbiota status, the health status, and the bioavailability and pharmacokinetics of RSV.

Although the database of human clinical studies on the website clinicaltrials.gov shows a number of clinical trials, most of which have evaluated the safety, bioavailability, pharmacokinetics, and tolerability of RSV, the number of studies to examine its efficacy in certain types of cancers is much smaller (Xiao et al. Citation2018). Future investigations would be required for the application of RSV to human diseases, including cancer.

Comparison of cancer site-specific effects based on observational epidemiological studies

lists the results of human studies on the cancer site-specific effects of the consumption of coffee, green tea, wine, and/or their major polyphenols, including whether their consumption can reduce cancer risk. In the case of curry/curcumin, most of the human studies have been limited to clinical trials; thus, it is difficult to evaluate their effects, resulting in the exclusion of data for curcumin from .

Table 1. Comparison of anticancer effects in observational epidemiology studies of coffee, tea, and wine consumption.

Although the consumption of these drinks appears beneficial in CRC, there are some cancer-specific differences in the effects among the intakes of these drinks. Coffee consumption may have a higher possibility to reduce the risk of endometrial cancer compared with consumption of tea and wine, as well as offer protection from liver and skin cancers. More recently, Pauwels and Volterrani (Citation2021) reported on the epidemiological evidence showing that in postmenopausal women, coffee intake was inversely associated with the risk of hepatocellular carcinoma (HCC) and, to a lesser extent, the risk of BCa. However, coffee consumption may specifically increase the risks of bladder and some types of blood cancer. Tea consumption may have beneficial effects against bladder, breast, gastric, and prostate cancers and may not increase the risk of any cancer. Wine consumption may be useful for reducing the risks of bladder cancer, but there is a possibility that it may increase the risk of breast and esophageal cancers.

At present, it is not clear what is the reason for these differences and future studies focusing on this issue must be performed.

Mechanism of anticancer effects of CGA, CUR, EGCG, and RSV

The results of a large number of animal and cell experiments have provided evidence to support the anticancer effects of CGA, CUR, EGCG, and RSV (Hayakawa et al. Citation2020; Lczbiński and Bukowska Citation2022; Yang and Wang Citation2016). Previously, we proposed a common anticancer mechanism for CGA and EGCG, stemming from their action as either antioxidants or prooxidants ( and , respectively) (Hayakawa et al. Citation2020; Hayakawa et al. Citation2016). These two polyphenols have common properties, in that they can activate adenosine monophosphate (AMP)-activated protein kinase (AMPK) and downregulate NF-κB via the modulation of ROS (). In view of the similar properties of these four polyphenols, we may expect similar mechanism for CUR and RSV, both of which are known to have antioxidant and prooxidant activities, and can activate AMPK and downregulate NF-κB () (Hayakawa et al. Citation2020).

Figure 2. Potential mechanisms whereby CGA, CUR, EGCG, and RSV exert anticancer effects by downregulating ROS. miRs written in red and blue are upregulated and downregulated by polyphenols, respectively. miRs in the yellow and green balloon can upregulate and downregulate the corresponding target, respectively.

Figure 2. Potential mechanisms whereby CGA, CUR, EGCG, and RSV exert anticancer effects by downregulating ROS. miRs written in red and blue are upregulated and downregulated by polyphenols, respectively. miRs in the yellow and green balloon can upregulate and downregulate the corresponding target, respectively.

Figure 3. Potential mechanisms whereby CGA, CUR, EGCG, and RSV exert anticancer effects by generating ROS. miRs written in red and blue are upregulated and downregulated by polyphenols, respectively. miRs in the yellow and green balloon can upregulate and downregulate the corresponding target, respectively.

Figure 3. Potential mechanisms whereby CGA, CUR, EGCG, and RSV exert anticancer effects by generating ROS. miRs written in red and blue are upregulated and downregulated by polyphenols, respectively. miRs in the yellow and green balloon can upregulate and downregulate the corresponding target, respectively.

Table 2. Modulatory effects of CGA, CUR, EGCG, and RSV on ROS, AMPK, and NF-κB.

In and , illustration of the ROS-mediated pathways through which these dietary polyphenols exert their anticancer effects is presented on the basis of our previous papers and other studies (Abadi et al. Citation2021b; Hayakawa et al. Citation2020; Hayakawa et al. Citation2016; Ohishi et al. Citation2021; Q. Xu et al. Citation2020), with some modifications. Recently, IL-8 has been shown to downregulate phosphatase tensin homolog deleted on chromosome 10 (PTEN) (Abadi et al. Citation2021b; Q. Xu et al. Citation2020), suggesting that the IL-8/PTEN axis could be incorporated into these figures based on the findings that these four dietary polyphenols can downregulate IL-8 (Kumar et al. Citation2017; Latruffe et al. Citation2015; Sordillo and Helson Citation2015; Takikawa et al. Citation2002) and activate PTEN (Meng et al. Citation2019; Qin et al. Citation2020; Vukelic et al. Citation2018; Z. Wang et al. Citation2020). Thus, the NF-κB/IL-8/PTEN/phosphatidylinositol-3-kinase (PI3K)/Akt axis might be operating in the ROS-mediated anticancer pathways, as shown in and .

At present, it is not clear which factor(s) directs the polyphenols to act as either an antioxidant or a prooxidant, although the cellular concentrations of metallic ions and polyphenols may be such factors (Hayakawa et al. Citation2020).

Modulation of miR by CGA, CUR, EGCG, and RSV

The translation of mRNA into protein is modulated by ncRNAs, which include miRs and long ncRNAs. The anticancer effects of plant polyphenols have been reported to be affected by these RNAs (Yi et al. Citation2019). The involvement of long ncRNAs in polyphenol-mediated anticancer effects has been comprehensively reviewed in detail by Yi et al. (Citation2019); therefore, we have focused here on the modulation of anticancer effects by miRs.

Approximately 30% of human mRNA expression related to cell growth, differentiation, and apoptosis is believed to be controlled by miRs (Z. Fu et al. Citation2021). The expression of some types of miRs may differ significantly between normal tissues and tumor tissues. Given their differential roles in cancer cells, miRs can be divided into oncogenic or tumor-promoting miRs (oncomiRs) and tumor-suppressing miRs, with any imbalances between them contributing to carcinogenesis, cancer invasion, and metastasis (Z. Fu et al. Citation2021). Differential expression of the same miRs may be seen among different cancer types, as exemplified by miR-27a, which is upregulated in PCa (Fletcher et al. Citation2012) and downregulated in acute leukemia cells (Scheibner et al. Citation2012).

The examples of the modulatory effects of CGA, CUR, EGCG, and RSV on cancer-related miRs are listed in and . In , data are presented on the modulatory effects that have been reported for only one of these polyphenols but not for others. The inconsistent results among these polyphenols may have arisen from experimental differences, including those of the cell types used and between the cell and animal experiments, which are not reflected in these tables. For example, CUR was reported to upregulate miR-34a in CRC, but downregulate it in esophageal cancer (Hesari et al. Citation2019) (). miR-7-5p was shown to be upregulated and downregulated in human osteosarcoma MG-63 and U2OS cell lines, respectively, after treatment with EGCG (Zhu and Wang Citation2016) (). In addition, results from microarray analyses may need confirmation by qRT-PCR.

Table 3. miRs that can be modulated by different dietary polyphenols.

Table 4. miRs for which modulation by only one of the four polyphenols is available.

shows that all four polyphenols can modulate miR-21 and three polyphenols can modulate eight miRs: miRs-16, 20a, 25, 34a, 93, 106 b, 145, and 200c. CUR, EGCG, and RSV upregulate miR-16, 34a, 145, and 200c, but downregulate miR-25. CGA, EGCG, and RSV downregulate miR-20a, 93, and 106b (). Data of many miRs have been available for only 2 polyphenols () or one polyphenol (). For an unknown reason, data for CGA are quite limited despite the numerous studies on anticancer effects of coffee and this polyphenol. It may be speculated that the lack in those data may reflect the situation under which authors considered the obtained results to be useless or not acceptable for publication. Such a decision would be feasible in case that the experimental results show no effect of a polyphenol treatment on miRs. Future comparative studies including those on CGA may lead to more convincing findings of the similarities and differences in the effects of polyphenols on miRs which might be useful for understanding the cancer site-specific effects based on epidemiological studies on coffee, green tea, and wine ().

The miRs for which data of modulation are available for at least 3 of these polyphenols are selected and shown in and , together with the modes of modulation by miRs in an attempt to connect the possible involvement of these miRs in the anticancer pathway triggered by these polyphenols depicted in and .

Table 5. Upregulation of tumor-suppressing miRs by CUR, EGCG, and RSV and their targets.

Table 6. Downregulation of tumor-promoting miRs by CGA, CUR, EGCG, and RSV and their targets.

Targets of tumor suppressor miRs upregulated by CUR, EGCG, and RSV

CUR, EGCG, and RSV can upregulate miR-16, 34a, 145, and 200c, which are known as tumor-suppressing miRs (Z. Fu et al. Citation2021; Zeng et al. Citation2021) ( and ). These targets are discussed for contribution to the polyphenol’s anticancer effects.

Targets of miR-16

Tsang and Kwok (Citation2010) used microarray analysis and found that EGCG upregulates the expression of 13 miRs and downregulates of 48 miRs in human hepatoma HepG2 cells. miR-16 is one of the upregulated miRs, and one of its target genes was confirmed to be anti-apoptotic protein Bcl-2. EGCG induced apoptosis and downregulated Bcl-2 in these cells. Transfection with commercially available anti-miR-16 inhibitor suppressed miR-16 expression and suppressed the EGCG induced downregulation of Bcl-2. Similarly, Yang et al. (Citation2010) demonstrated that CUR reduced the expression of Bcl-2 by upregulating the expression of miR-15a and miR-16 in MCF-7 cells. Hagiwara et al. (Citation2012) found that RSV promotes the expression and activity of Argonaute2, a central RNA interference component, which inhibits BCa stem-like cell characteristics by increasing the expression of a number of tumor-suppressive miRNAs, including miR-16, 141, 143, and 200c.

Targets of miR-34a

miR-34a is known as a tumor suppressor miR and bioinformatic analyses suggest that vascular endothelial growth factor (VEGF) is a target of miR-34a. The phosphorylation of FAK at 397 sites was downregulated in CRC cells, which have overexpressed miR-34a, and phosphorylation in miR-34a stable cell lines was completely rescued by extra VEGF treatment (D. Zhang et al. Citation2014).

Many cancer types, including human osteosarcoma, exhibit elevated expression of survivin. Chen et al. (Citation2016) found that human osteosarcoma U2OS and Saos-2 cells have high expression levels of survivin, the knockdown of which causes the inhibition of cell proliferation, cell cycle arrest at the G2/M phase, and the induction of apoptosis. miR-34a and miR-203 target survivin and downregulate its expression, leading to the suppression of the maintenance and proliferation of osteosarcoma cells.

Shanesazzade et al. (Citation2018) showed that 1-methyl-4-phenylpyridinium-treated human SH-SY5Y neuronal cells underwent oxidative stress and apoptosis, together with the upregulation of miR-34a and the downregulation of Bcl-2, suggesting that the miR-34a/Bcl-2 axis was directly correlated with oxidative stress and apoptosis in SH-SY5Y cells.

Yao et al. (Citation2021) observed that RSV increased the expression of miR-34a in ovarian cancer cells and activated the apoptotic pathway by suppressing Bcl-2-dependent signaling. The knockdown of miR-34a attenuated the antitumor activity of RSV in these cells. Bcl-2 overexpression canceled the anticancer effects of RSV. Similarly, Kumazaki et al. (Citation2013) found that EGCG and RSV caused a decrease in the number of viable cells and induced apoptosis in three human colon cancer cell lines with the suppression of the PI3K/Akt signaling pathway. RSV increased the intracellular expression level of miR-34a, which downregulated the target gene E2F3 and its downstream Sirtuin1 (SIRT1), resulting in growth inhibition. L. Li et al. (Citation2013) demonstrated that miR-34a can downregulate SIRT1 and Bcl-2 directly in breast cancer cells.

Subramaniam et al. (Citation2012) “surprisingly” observed decreased but not increased expression of miR-34a in response to CUR. According to these authors, one of the explanations for this discrepancy may be the difference in the cell types used, because they studied esophageal cancer cells with nonfunctional p53 protein, which is related to miR-34a expression. They also observed upregulation of tumor suppressor miR-let-7a. This modulation may overcome the downregulating effect of miR-34a for CUR to exert the anticancer effect.

Targets of miR-145

miR-145 and miR-200c are downregulated in nasopharyngeal cancer stem cells. Shen et al. (Citation2013) found that RSV impeded cancer stem cell properties of nasopharyngeal carcinoma via the activation of p53 and induced miR-145 and miR-200c. These authors suggested the link between these miRs and p53.

The p21 activated kinase 4 (PAK4) is an upstream kinase for activation of ERK1/2 (Ramos-Alvarez et al. Citation2020). Wang et al. (Citation2012) demonstrated that miR-145 targets a putative binding site in the 3′-UTR of PAK4 and its abundance is inversely associated with miR-145 expression in colon cancer cells. The restoration of miR-145 by mimics in colon cancer cells significantly attenuated cell growth through downregulation of the PAK4/Raf/MEK/ERK1/2 pathway.

The epidermal growth factor receptor (EGFR) is a growth factor receptor that is frequently upregulated in various cancers, including lung cancer, and can be a therapeutic target. Cho et al. (Citation2011) found that miR-145 directly targets EGFR. The transfection with miR-145 inhibited the proliferation of lung adenocarcinoma cells and was correlated strongly with the downregulation of EGFR, suggesting that miR-145 acts as a tumor suppressor in lung cancer by targeting EGFR.

Targets of miR-200c

The aberrant activation of Kirsten rat sarcoma viral oncogene (KRAS) causes the abnormal activation of downstream signaling pathways, including ERK1/2 (Cagnol and Rivard Citation2013). Song et al. (Citation2015) showed that low miR-200c expression is associated with poor overall survival and disease-free survival and miR-200c inhibits Akt and ERK pathways by directly targeting KRAS. The inhibition of KRAS by miR-200c suppressed the proliferation and survival of BCa cells in vitro and in vivo, suggesting the anticancer properties of miR-200c.

VEGF receptor-2 (VEGFR2) is a major cell-surface receptor for VEGF, and VEGF/VEGFR2 signaling is critical for angiogenesis (Cebe-Suarez et al. Citation2006). In a study of biochemical assays, Shi et al. (Citation2013) demonstrated that miR-200c directly targets VEGFR2 and transfection with miR-200c radiosensitized A549 cells by targeting the VEGFR2/VEGF pathway, leading to inhibition of its downstream survival signaling transduction and angiogenesis.

Mitogen-inducible gene 6 (MIG6) is a protein that inhibits the EGFR through a classic feedback mechanism (Park et al. Citation2015). In a TGF-β-induced model of the epithelial-mesenchymal transition (EMT), Izumchenko et al. (Citation2014) found that the inhibition of the miR-200 family results in the upregulation of MIG6. They demonstrated that the ratio of the expression of MIG6 and miR200c was found to be correlated with EMT and resistance to erlotinib in lung cancer in vivo, suggesting that the MIG6/miR200 ratio could be a predictive biomarker of the response of lung cancer to EGFR inhibitors.

Targets of oncogenic miRs downregulated by CGA, CUR, EGCG, and RSV

CGA, EGCG, and RSV can downregulate miR-20a, 21, 93, and 106b, which are known as tumor-promoting miRs or oncomiRs (Abadi et al. Citation2021b; Amirfallah et al. Citation2021; Chen et al. Citation2021b; Z. Fu et al. Citation2021; Xiao et al. Citation2021) ( and ). CUR, EGCG, and RSV were reported to downregulate oncogenic miR-25 ( and ).

Targets of miR-20a

He et al. (Citation2013) demonstrated that miR-20a inhibits U937 cell differentiation induced by HIF-1a and promotes cell proliferation in vivo. The ectopic expression of miR-20a and miR-17 reduced the protein levels of p21 and STAT3 expression, suggesting that p21 and STAT3 are direct targets of these miRs.

Yuan et al. (Citation2019) found the differential expression of miR-19b and miR-20a, members of the crucial oncogene miR-17 − 92 cluster, between patients with multiple myeloma and normal controls. miR-19b/20a promoted cell proliferation and migration, inhibited cell apoptosis, and altered cell cycles in multiple myeloma cells. The transfection of miR-19b/20a reduced the expression of PTEN, indicating that PTEN is a direct target of miR-19b/20a. The overexpression of miR-19b/20a reversed the effect of PTEN and lentivirus-mediated delivery of miR-20a enhanced tumor growth in a murine xenograft model.

Several oncogenic miRs are known to promote cancer growth and invasion via PTEN downregulation, leading to activation of the PI3K/Akt pathway, which promotes cancer growth (Abadi et al. Citation2021b). Thus, the suppression of these miRs would result in downregulation of this pathway, and then exert anticancer effects.

Targets of miR-21

A study using a miRNA microarray found that miR-21 was overexpressed in HCC tumors and tumor cell lines (Meng et al. Citation2007). Transfection with precursor miR-21 increased tumor cell proliferation, migration, and invasion, and normal hepatocytes transfected with antisense miRNA displayed the upregulation of PTEN and the downregulation of Akt and focal adhesion kinase (FAK). Transfection with precursor miR-21 into normal hepatocytes led to the upregulation of FAK phosphorylation and the expression of MMP9, which are involved in cell migration and invasion.

W. Zhang et al. (Citation2014) found that CUR inhibited cell proliferation and induced apoptosis in human lung epithelial A549 cells and decreased miR-21 expression when compared to untreated cells. The protein level of PTEN was elevated by CUR and transfection of miR-21 mimic into these cells reversed the growth suppression and apoptosis caused by CUR. Sheth et al. (Citation2012) demonstrated that RSV reduced the expression of various prostate-tumor associated miRs including miR-21 in human PCa PC-3M-MM2 cells with association of reduced cell viability, migration and invasiveness. In the SCID mouse xenograft model of PCa, oral administration of RSV inhibited the tumor growth and decreased the number of metastatic lung lesions which were associated with reduced miR-21 expression and phosphorylation of Akt.

Targets of miR-25

Gordon et al. (Citation2015) demonstrated that carcinogen benzo[a]pyrene upregulated the expression of seven p53-targeting miRNAs (miR-15a, 16, 25, 92, 125 b, 141, and 200a) in multiple myeloma cells and that 2,3,7,8-tetrachlorodibenzo-ρ-dioxin upregulated miR-25 and miR-92. They found that EGCG reduced the expression of four of these miRNAs: miR-25, 92, 141, and 200a, suggesting anticancer effect of EGCG.

Kumar et al. (Citation2011) found that miR-25 and miR-30d directly target the 3′-UTR of TP53 to downregulate p53 protein levels, leading to a reduction in the expression of genes transcriptionally activated by p53. The inhibition of miR-25 expression increased p53 expression and elevated cellular apoptosis in several cell lines, including human colorectal carcinoma HCT116 cells, suggesting that polyphenols downregulating miR-25 would have an anticancer effect by promoting cancer cell death.

Ding et al. (Citation2018) found that the overexpression of miR-25 by the transfection of miR promoted the migration and invasion of human nonsmall-cell lung cancer (NSCLC), whereas chemically synthesized antagonistic RNA of miR-25 downregulated cell migration and invasion. They also showed that miR-25 activated the ERK signaling pathway by directly targeting Krüppel-like factor 4, which has lower expression in tissues from patients with NSCLC than in control patients.

A study to examine the effects and the potential mechanism of miR-25 in doxorubicin (DOX)-induced cardiac injury found that DOX increased the level of miR-25 and downregulated the expression of PTEN (Li et al. Citation2020). The overexpression of miR-25 using miR mimics aggravated DOX-induced apoptosis, ROS, and DNA damage in rat H9c2 cardiomyoblasts. In contrast, miR-25 inhibitor could alleviate the damage induced by DOX.

Targets of miR-93 and miR-106b

EGCG was shown to decrease expression of the oncogenic miR-93 and miR-106b in human neuroblastoma SH-SY5Y and SK-N-DZ cells. The overexpression of miR-93 decreased the efficacy of EGCG in the induction of apoptosis (Chakrabarti et al. Citation2013).

Estrogens are believed to play a causative role in BCa. Singh et al. (Citation2014) found that RSV decreased tumor incidence and increased the latency of 17β-estradiol-induced mammary tumors in a female rat model. The hormone treatment significantly increased the expression of miR-93, but its expression remained at control levels by RSV in 17β-estradiol-treated human MCF-10A cells.

Dhar et al. (Citation2015) demonstrated that RSV decreased the levels of endogenous as well as exogenously expressed miR-17, miR-20a, and miR-106b, by accompanying upregulation of PTEN in PCa DU145 and 22Rv1 cells expressing wild-type PTEN.

A miRNA microarray experiment demonstrated that the members of the miR-17 family, miR-20a, 93, and 106 b, were downregulated in a dose-dependent manner after exposure to CGA in Huh7 and H446 cells, and the results were confirmed by the qRT-PCR (Huang et al. Citation2019).

In human prostate LNCaP cells, a miR-93 inhibitor led to a decrease in the mRNA expression of androgen receptor and PSA compared with the control group (Mokhtari et al. Citation2020). The co-transfection of this inhibitor with EGCG caused a greater decrease in both the androgen receptor and PSA expression compared with the transfection without EGCG.

As miRNA-93 and 106 b are oncogenic factors that promote cancer growth and invasion via PTEN downregulation, leading to the activation of the PI3K/Akt pathway, which promotes cancer growth; consequently, the suppression of these miRs would result in the downregulation of this pathway to exert anticancer effects (Abadi et al. Citation2021b).

Anticancer effects of EGCG via the 67 kDa laminin receptor

Among dietary polyphenols, EGCG appears unique as it exhibits an anticancer pathway via the 67 kDa laminin receptor (67LR), which was discovered by Tachibana et al. (Citation2004). EGCG inhibits melanoma tumor growth by activating 67LR signaling. A miRNA microarray analysis showed that EGCG upregulated the expression of several let-7 family miRs through 67LR in melanoma cells; qRT-PCR confirmed the upregulation of let-7b () (Yamada et al. Citation2016). The EGCG induced upregulation of let-7b led to downregulation of high mobility group A2 (HMGA2), a target gene related to tumor progression. The activation of the 67LR-dependent cAMP/protein kinase A (PKA)/protein phosphatase 2 A (PP2A) signaling pathway is involved in the upregulation of let-7b expression induced by EGCG.

It can be speculated that this unique modulation contributes to the anticancer effects of EGCG, in addition to those occurring through the ROS-mediated signaling pathway ( and ), thereby explaining the finding that there is no distinct epidemiological evidence supporting the increased cancer risk for any types examined by green tea consumption ().

Concluding remarks

Epidemiological studies have shown that the consumption of coffee, green tea, wine, and curry may contribute to the reduced risk of a variety of cancer types. There are some cancer site-specific differences in the effects of their consumption (). For example, the risk of bladder cancer may be reduced by the consumption of tea or wine, whereas coffee consumption may increase this risk. Wine consumption may be unfavorable for BCa, but coffee and tea consumption appear beneficial. Further well-controlled studies are required to identify the reasons for these differences.

Many animal and cell-based experiments have provided the mechanisms through which dietary polyphenols exert their anticancer effects. Among them, the mechanisms in which ROS are involved appear to be the most likely candidate ( and ). CGA, CUR, EGCG, and RSV are all known to act as antioxidants and to activate AMPK by downregulating ROS (). They are also known to generate ROS and downregulate NF-κB (). These modulations can activate or downregulate the signaling pathway, leading to the prevention of carcinogenesis and cancer development.

Recent studies have revealed that these polyphenols can modulate the expression of miRs that affect protein synthesis and degradation in normal and cancer tissues. The accumulated data show that all four dietary polyphenols can downregulate tumor-promoting miR-21. CUR, EGCG, and RSV can upregulate four tumor-suppressing miRs, miR-16, 34a, 145, and 200c, while they downregulate a tumor-promoting miR-25. CGA, EGCG, and RSV downregulate tumor-promoting miR-20a, 93, and 106 b. These effects resulting from the modulation of miRs may affect ROS-mediated pathways, leading to the enhanced anticancer effects exerted by these polyphenols ( and ). miRs other than these miRs may also have a role to modify ROS-mediated or other anticancer pathways and some modulatory effects may contribute to the differences in cancer site-specific effects among intakes of coffee, green tea, and wine (). More precise analysis is needed to know whether the differences in modulation of miRs exerted by these polyphenols is involved in this issue.

It is interesting to note that the 10 miRs discussed here (miR-16, 20a, 21, 25, 34a, 93, 106 b, 145, 200c, and let7b) are promising candidates for the development of gene therapy drugs and that some potential drugs targeting these miRs have been developed. For example, trypaflavine, and kanamycin A are inhibitors targeting miR-21, and let-7, respectively (Z. Fu et al. Citation2021). Moreover, studies of miR-16 and 34a for drug development are in progress (Z. Fu et al. Citation2021).

Similar to CGA, CUR, EGCG, and RSV, other polyphenols such as oleacein, found in olive oil and its leaves (Lozano-Castellon et al. Citation2020), piceatannol found in grapes, passion fruit, and blueberries (Cao et al. Citation2020), and proanthocyanidin, found in variety of plants and their fruits (Zhu Citation2019), are also attracting attention because of their positive effects on health including anticancer activity (Cao et al. Citation2020; Emma et al. Citation2021; Zhu Citation2019).

As these polyphenols are known to have beneficial effects not only in cancer, but also in other diseases, such as obesity, diabetes, cardiovascular diseases, and neurodegenerative disease, the future analysis of miRs modulated by polyphenols may also provide useful information for the development of drugs against these diseases.

Abbreviations
67LR =

67 kDa laminin receptor
ACF =

aberrant crypt foci
AMP =

adenosine monophosphate
AMPK =

AMP-activated protein kinase
BCa =

breast cancer
CGA =

chlorogenic acid
CI =

confidence interval
CRC =

colorectal cancer
CUR =

curcumin
DOX =

doxorubicin
EGCG =

epigallocatechin gallate
EGFR =

epidermal growth factor receptor
EMT =

epithelial-mesenchymal transition
FAK =

focal adhesion kinase
GTC =

green tea catechins
HCC =

hepatocellular carcinoma
HMGA2 =

high mobility group A2
HPV =

human papilloma viruses
HR =

hazard ratio
IL-8 =

Interleukin-8
RASSF-1α =

Ras-association domain family-1α
KRAS =

Kirsten rat sarcoma viral oncogene
MIG6 =

mitogen-inducible gene 6
miR =

miRNA
ncRNAs =

noncoding RNAs
NSCLC =

nonsmall-cell lung cancer
OR =

odds ratio
PAK4 =

p21 activated kinase 4
PCa =

prostate cancer
PI3K =

phosphatidylinositol-3-kinase
PKA =

protein kinase A
PP2A =

protein phosphatase 2A
PSA =

prostate cancer specific antigen
PTEN =

phosphatase tensin homolog deleted on chromosome 10
RCT =

randomized controlled trial
ROS =

reactive oxygen species
RR =

relative risk
RSV =

resveratrol
SIRT1 =

sirtuin1
TCa =

thyroid cancer
TGF-β =

transforming growth factor-β
TNF-α =

tumor necrosis factor-α
VEGF =

vascular endothelial growth factor
VEGFR2 =

VEGF receptor-2

Declaration of interest statement

The authors declare no conflicts of interest associated with this manuscript.

Funding

The author(s) reported there is no funding associated with the work featured in this article.

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