Genistein and biochanin A inhibit the growth of human prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation

Greg Peterson,

Greg Peterson

Departments of Biochemistry and Pharmacology, University of Alabama at Birmingham, Birmingham

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Stephen Barnes,

Corresponding Author

Stephen Barnes

Departments of Biochemistry and Pharmacology, University of Alabama at Birmingham, Birmingham

Department of Pharmacology, University of Alabama at Birmingham, Birmingham, AL 35294-0019Search for more papers by this author

Greg Peterson,

Greg Peterson

Departments of Biochemistry and Pharmacology, University of Alabama at Birmingham, Birmingham

Search for more papers by this author

Stephen Barnes,

Corresponding Author

Stephen Barnes

Departments of Biochemistry and Pharmacology, University of Alabama at Birmingham, Birmingham

Department of Pharmacology, University of Alabama at Birmingham, Birmingham, AL 35294-0019Search for more papers by this author

First published: 1993

https://doi.org/10.1002/pros.2990220408

Citations: 311

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Abstract

The effect of the isoflavones, genistein, daidzein, and biochanin A on the growth of the LNCaP and DU-145 human prostate cancer cell lines has been examined. Genistein and biochanin A, but not daidzein, inhibit both serum and EGF-stimulated growth of LNCaP and DU-145 cells (IC50 values from 8.0 to 27 μg/ml for serum and 4.3 to 15 μg/ml for EGF), but have no significant effect of the EGF receptor tyrosine autophosphorylation. In contrast, tyrphostin 25, a specific EGF receptor tyrosine kinase inhibitor, inhibits EGF-stimulated growth and EGF receptor tyrosine autophosphorylation in these whole cells, but does not inhibit serum-stimulated growth. These data suggest that the mechanism of action of genistein and biochanin A does not depend on inhibition of EGF receptor tyrosine autophosphorylation, but on a more distal event in the EGF receptor-mediated signal transduction cascade. © 1993 Wiley-Liss, Inc.

References

1 Tominaga S: Cancer incidence in Japanese in Japan, Hawaii, and Western United States. Natl Cancer Inst Monogr 69: 83–92, 1985.

CASPubMedGoogle Scholar
2 Dunn JE: Cancer epidemiology in populations of the United States with emphasis on Hawaii and California and Japan. Cancer Res 35: 3240–3245, 1975.

CASPubMedWeb of Science®Google Scholar
3 Donn AS, Muir CS: Prostatic cancer: Some epidemiological factors. Bulletin de Cancer 72: 381–390, 1985.

CASPubMedWeb of Science®Google Scholar
4 Barnes S, Grubbs C, Setchell KDR, Carlson J: Soybeans inhibit mammary tumors in models of breast cancer. Prog Clin Biol Res 347: 239–253, 1990.

CASPubMedWeb of Science®Google Scholar
5 Peterson G, Barnes S: Genistein inhibition of the growth of human breast cancer cells: Independence from estrogen receptors and the multi-drug resistance gene. Biochem Biophys Res Commun 179: 661–667, 1991.
10.1016/0006-291X(91)91423-A
CASPubMedWeb of Science®Google Scholar
6 Setchell KDR, Borriello SP, Hulme, Dirk DN, Axelson M: Nonsteroidal estrogens of dietary origin: Possible roles in hormone dependent disease. Am J Clin Nutr 40: 569–578, 1984.
10.1093/ajcn/40.3.569
CASPubMedWeb of Science®Google Scholar
7 Akiyama T, Ishida J, Nakagawa S, Ogawara S, Watanabe S, Itoh N, Shiyuba M, Fukiyama Y: Genistein, a specific inhibitor of tyrosine-specific protein kinases. J Biol Chem 262: 5592–5595, 1987.
10.1016/S0021-9258(18)45614-1
CASPubMedWeb of Science®Google Scholar
8 Hill TD, Dean NM, Mordan LJ, Lau AF, Kanemitsu MY, Boynton AL: PDGF-induced activation of phospholipase C is not required for induction of DNA synthesis. Science 248: 1660–1663, 1990.
10.1126/science.2163545
CASPubMedWeb of Science®Google Scholar
9 Kuriu A, Ikeda H, Kanakura Y, Griffin JD, Drucker B, Yagura H, Kitayama H, Ishikawa J, Nishiura T, Kanayama Y: Proliferation of human myeloid leukemia cell line associated with the tyrosine-phosphorylation and activation of the proto-oncogene c-kit product. Blood 78: 2834–2840, 1991.

CASPubMedWeb of Science®Google Scholar
10 Trevillyan JM, Lu Y, Alturu D, Phillips CA, Bjorndahl JM: Differential inhibition of T cell receptor signal transduction and early activation events by a selective inhibitor of protein tyrosine kinase. J Immunol 145: 3223–3330, 1990.

CASPubMedWeb of Science®Google Scholar
11 Honma Y, Okabe-Kado J, Kasaukabe T, Hozumi M, Umezawa K: Inhibition of abl oncogene tyrosine kinase induces erythroid differentiation of human myelogenous leukemia K-562 cells. Jpn J Cancer Res 81: 1132–1136, 1990.
10.1111/j.1349-7006.1990.tb02524.x
CASPubMedWeb of Science®Google Scholar
12 Connally JM, Rose DP: Production of epidermal growth factor and transforming growth factor-a by the androgen-responsive LNCaP human prostate cancer cell line. Prostate 16: 1235–1241, 1990.

Google Scholar
13 Connally JM, Rose DP: Secretion of epidermal growth factor and related polypeptides by the DU-145 human prostate cancer cell line. Prostate 15: 177–186, 1989.
10.1002/pros.2990150211
PubMedWeb of Science®Google Scholar
14 Schuurmans ALG, Bolt J, Mulder E: Androgens stimulate both growth rate and epidermal growth factor receptor activity of the human prostate tumor cell LNCaP. Prostate 12: 55–63, 1988.
10.1002/pros.2990120108
CASPubMedWeb of Science®Google Scholar
15 Chen WS, Lazar CS, Poenie M, Tsien RY, Gill GN, Rosenfeld MG: Requirement for intrinsic protein tyrosine kinase in the immediate and late actions of the EGF receptor. Nature 328: 820–823, 1987.
10.1038/328820a0
CASPubMedWeb of Science®Google Scholar
16 Gazit A, Yaish P, Gilon C, Levitski A: Tyrphostins I: Synthesis and biological activity of protein tyrosine kinase inhibitors. J Med Chem 32: 2344–2352, 1989.
10.1021/jm00130a020
CASPubMedWeb of Science®Google Scholar
17 Lowry OH, Rosebrough NJ, Farr AL, Randall RJ: Protein measurement with folin phenol reagent. J Biol Chem 193: 265–275, 1951.
10.1016/S0021-9258(19)52451-6
CASPubMedWeb of Science®Google Scholar
18 Binder LI, Frankfurter A, Rebhun LI: The distribution of tau in the central nervous system. J Cell Biol 101: 1371–1378, 1985.
10.1083/jcb.101.4.1371
CASPubMedWeb of Science®Google Scholar
19 Okura A, Arakawa H, Oka H, Yoshinari T, Monden Y: Effect of genistein on topoisomerase activity and on the growth of [val 12] Ha-ras-transformed NIH-3T3 cells. Biochem Biophys Res Commun 157: 183–189, 1988.
10.1016/S0006-291X(88)80030-5
CASPubMedWeb of Science®Google Scholar
20 Linassier C, Pierre M, LePecq JB, Pierre J: Mechanisms of action in NIH-3T3 cells of genistein, an inhibitor of EGF receptor tyrosine kinase activity. Biochem Pharmacol 39: 187–193, 1990.
10.1016/0006-2952(90)90664-7
CASPubMedWeb of Science®Google Scholar
21 Payne MD, Rossomando AJ, Martino J, Erickson AK, Her J-H, Shabanowitz J, Hunt DF, Weber MJ, Sturgill TW: Identification of the regulatory phosphorylation sites in pp42/ mitogen activated protein kinase (MAP kinase). EMBO J 10: 885–892, 1991.
10.1002/j.1460-2075.1991.tb08021.x
CASPubMedWeb of Science®Google Scholar
22 Anderson NG, Mailer JL, Tonks NK, Sturgill TW: Requirement for integration of signals from two distinct phosphorylation pathways for activation of MAP kinase. Nature 343: 651–653, 1990.
10.1038/343651a0
CASPubMedWeb of Science®Google Scholar
23 Imoto M, Yamashita T, Sawa H, Kurasawa S, Naganawa H, Takeuch T, Boa-quan Z, Umezawa K: Inhibition of cellular phosphatidylinositol turnover by psi-tectorigenin. FEBS Lett 230: 43–46, 1988.
10.1016/0014-5793(88)80638-0
CASPubMedWeb of Science®Google Scholar
24 Makishma M, Homa Y, Hozumi M, Sampi K, Hattori M, Umezawa K, Motoyoshi K, Saitama K: Effects of inhibitors of protein kinase activity and/or phosphatidylinositol turnover on differentiation of some human myelomonocytic leukemia cells. Leuk Res 15: 701–708, 1991.
10.1016/0145-2126(91)90072-2
PubMedWeb of Science®Google Scholar
25 Constantinou A, Kiguchi K, Huberman E: Induction of differentiation and strand breakage in human HL-60 and K-562 leukemia cells by genistein. Cancer Res 50: 2618–2624, 1990.

CASPubMedWeb of Science®Google Scholar
26 Markovits J, Linassier C, Fosse P, Couprie J, Jaquemin-Sablon A, Pecq JB, Larson AK: Inhibitory effects of the tyrosine kinase inhibitor genistein on mammalian DNA topoisomerase II. Cancer Res 49: 5111–5117, 1989.

CASPubMedWeb of Science®Google Scholar
27 Schuurmans ALG, Bolt J, Veldscholte J, Mulder E: Stimulatory effects of antiandrogens on LNCaP human prostate tumor cell growth, EGF-receptor level and acid phosphatase secretion. J Steroid Biochem Mol Biol 37: 849–853, 1990.
10.1016/0960-0760(90)90431-J
CASPubMedWeb of Science®Google Scholar
28 Mulder E, van Loon D, de Boer W, Schuurmans ALG, Bolt J, Voorhorst MM, Kuiper GGJM, Brinkman AO: Mechanism of androgen action: Recent observations on the domain structure of androgen receptors and the induction of EGF-receptors by androgens in prostate tumor cells. J Steroid Biochem Mol Biol 32: 151–156, 1989.
10.1016/0022-4731(89)90156-8
CASPubMedWeb of Science®Google Scholar
29 Axelson M, Sjovall J, Gustafson B, Setchell KDR: Soya—a dietary source of the non-steroidal oestrogen equol in humans and animals. J Endocrin 102: 49–56, 1984.
10.1677/joe.0.1020049
CASPubMedWeb of Science®Google Scholar

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Volume22, Issue4

1993

Pages 335-345

Genistein and biochanin A inhibit the growth of human prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation

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Genistein and biochanin A inhibit the growth of human prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation

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