The Effects of Bioactive Food Components on p53 Pathway in Cancer Prevention

Recent research has shown that a variety of bioactive food components, including both essential and nonessential nutrients, may influence cancer risk and tumor cell behavior by modulating the p53 tumor-suppressor gene pathway. The impact the dietary components have on this pathway likely depends on a host of genetic events that determine whether cells die or proliferate. This determination is made during the cell cycle progression that involves the actions of multiple genes including p21, bax, and bcl-2 as well as p53. Evidence from in vitro studies already exists linking a number of nutrients, including butyrate (an intestinal product of fiber), resveratrol (a phytoalexin found in red grapes), genistein (an isoflavonoid found in soybeans), and epigallocatechin-3-gallate (a polyphenol found in tea), to an increase in apoptosis or a decrease in proliferation of tumor cells. Although these results are promising, more research should be done to examine the efficacy of these compounds and to determine the optimal nutrient concentration needed to effectively prevent human cancers.

[1]  K. Kinzler,et al.  Role of BAX in the apoptotic response to anticancer agents. , 2000, Science.

[2]  S. Gupta,et al.  Growth inhibition, cell-cycle dysregulation, and induction of apoptosis by green tea constituent (-)-epigallocatechin-3-gallate in androgen-sensitive and androgen-insensitive human prostate carcinoma cells. , 2000, Toxicology and applied pharmacology.

[3]  R. Lutz,et al.  Role of the BH3 (Bcl-2 homology 3) domain in the regulation of apoptosis and Bcl-2-related proteins. , 2000, Biochemical Society transactions.

[4]  Shigeomi Shimizu,et al.  Bcl‐2 family: Life‐or‐death switch , 2000, FEBS letters.

[5]  Jen-kun Lin,et al.  Inhibition of cyclin‐dependent kinases 2 and 4 activities as well as induction of cdk inhibitors p21 and p27 during growth arrest of human breast carcinoma cells by (−)‐epigallocatechin‐3‐gallate , 1999, Journal of cellular biochemistry.

[6]  S. Hecht,et al.  Tobacco smoke carcinogens and lung cancer. , 1999, Journal of the National Cancer Institute.

[7]  Z. Darżynkiewicz,et al.  Resveratrol increases nitric oxide synthase, induces accumulation of p53 and p21(WAF1/CIP1), and suppresses cultured bovine pulmonary artery endothelial cell proliferation by perturbing progression through S and G2. , 1999, Cancer research.

[8]  Yiwei Li,et al.  Induction of apoptosis in breast cancer cells MDA-MB-231 by genistein , 1999, Oncogene.

[9]  S. Gupta,et al.  Prostate cancer chemoprevention by green tea. , 1999, Seminars in urologic oncology.

[10]  S. Archer,et al.  Histone acetylation and cancer. , 1999, Current opinion in genetics & development.

[11]  M. Katsuki,et al.  Inhibition of benzo[a]pyrene-induced mutagenesis by (-)-epigallocatechin gallate in the lung of rpsL transgenic mice. , 1999, Carcinogenesis.

[12]  Weiya Ma,et al.  Resveratrol suppresses cell transformation and induces apoptosis through a p53-dependent pathway. , 1999, Carcinogenesis.

[13]  R. Sadoul BCL-2 family members in the development and degenerative pathologies of the nervous system , 1998, Cell Death and Differentiation.

[14]  S. Meng,et al.  p21WAF1 is required for butyrate-mediated growth inhibition of human colon cancer cells , 1998 .

[15]  M. Katdare,et al.  Inhibition of aberrant proliferation and induction of apoptosis in pre-neoplastic human mammary epithelial cells by natural phytochemicals. , 1998, Oncology reports.

[16]  C. Paraskeva,et al.  Modulation of p53 expression in cultured colonic adenoma cell lines by the naturally occurring lumenal factors butyrate and deoxycholate , 1997, International journal of cancer.

[17]  S. Barnes The chemopreventive properties of soy isoflavonoids in animal models of breast cancer , 1997, Breast Cancer Research and Treatment.

[18]  A. Levine p53, the Cellular Gatekeeper for Growth and Division , 1997, Cell.

[19]  M. Mandal,et al.  Bcl-2 expression regulates sodium butyrate-induced apoptosis in human MCF-7 breast cancer cells. , 1996, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.

[20]  B. Evers,et al.  Induction of apoptosis in human gastric cancer by sodium butyrate. , 2000, Anticancer research.

[21]  F. D. de Gruijl Skin cancer and solar UV radiation. , 1999, European journal of cancer.

[22]  Yiwei Li,et al.  p53-independent apoptosis induced by genistein in lung cancer cells. , 1999, Nutrition and cancer.

[23]  C. Young,et al.  Resveratrol inhibits the expression and function of the androgen receptor in LNCaP prostate cancer cells. , 1999, Cancer research.

[24]  M. Madigan,et al.  Sodium butyrate modulates p53 and Bcl-2 expression in human retinoblastoma cell lines. , 1999, Oncology research.

[25]  Yiwei Li,et al.  Genistein-induced G2-M arrest, p21WAF1 upregulation, and apoptosis in a non-small-cell lung cancer cell line. , 1998, Nutrition and cancer.

[26]  J. Bushman Green tea and cancer in humans: a review of the literature. , 1998, Nutrition and cancer.

[27]  W. El-Deiry,et al.  Regulation of p53 downstream genes. , 1998, Seminars in cancer biology.