Curcumin: updated molecular mechanisms and intervention targets in human lung cancer

Int J Mol Sci. 2012;13(3):3959-3978. doi: 10.3390/ijms13033959. Epub 2012 Mar 22.

Abstract

Curcumin, a yellow pigment derived from Curcuma longa Linn, has attracted great interest in the research of cancer during the past decades. Extensive studies documented that curcumin attenuates cancer cell proliferation and promotes apoptosis in vivo and in vitro. Curcumin has been demonstrated to interact with multiple molecules and signal pathways, which makes it a potential adjuvant anti-cancer agent to chemotherapy. Previous investigations focus on the mechanisms of action for curcumin, which is shown to manipulate transcription factors and induce apoptosis in various kinds of human cancer. Apart from transcription factors and apoptosis, emerging studies shed light on latent targets of curcumin against epidermal growth factor receptor (EGFR), microRNAs (miRNA), autophagy and cancer stem cell. The present review predominantly discusses significance of EGFR, miRNA, autophagy and cancer stem cell in lung cancer therapy. Curcumin as a natural phytochemicals could communicate with these novel targets and show synergism to chemotherapy. Additionally, curcumin is well tolerated in humans. Therefore, EGFR-, miRNA-, autophagy- and cancer stem cell-based therapy in the presence of curcumin might be promising mechanisms and targets in the therapeutic strategy of lung cancer.

Keywords: EGFR; autophagy; cancer stem cell; curcumin; lung cancer; miRNA.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects
  • Autophagy / drug effects*
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Curcumin / pharmacology*
  • ErbB Receptors / antagonists & inhibitors
  • Humans
  • Lung Neoplasms / drug therapy*
  • MicroRNAs / antagonists & inhibitors
  • MicroRNAs / biosynthesis
  • Neoplastic Stem Cells / pathology
  • Signal Transduction / drug effects
  • Transcription Factors / biosynthesis*
  • Transcription Factors / metabolism

Substances

  • Antineoplastic Agents
  • MicroRNAs
  • Transcription Factors
  • EGFR protein, human
  • ErbB Receptors
  • Curcumin