Inhibition of proliferation and induction of apoptosis by genistein in colon cancer HT-29 cells.

Abstract

Genistein has multiple anticancer properties. However, its mechanisms of action and its molecular targets on human colon cells remain to be further elucidated. Here, we demonstrated that genistein reduced proliferation and induced G2/M phase arrest and apoptotic death in colon cancer HT-29 cells. We then investigated the effects of genistein on molecules that regulate apoptosis and cell cycle progress. Genistein increased expression of Bax and p21WAF1 and slightly decreased Bcl-2 level. Our results demonstrated that genistein inhibited the viability of human colon cancer HT-29 cell via induction of apoptosis mainly through regulation of p21WAF1 and Bax/Bcl-2 expression. These data suggested a role of genistein in prevention of colon tumor and might reduce colon tumor growth.

• Authors: Zengli Yu, Wenjie Li, Fuyun Liu
• Journal: Cancer letters (Cancer Lett) Vol. 215 Issue 2 Pg. 159-66 (Nov 25 2004) ISSN: 0304-3835 [Print] Ireland
• PMID: 15488634 (Publication Type: Journal Article)

Chemical References

• Antineoplastic Agents
• BAX protein, human
• CDKN1A protein, human
• Cell Cycle Proteins
• Cyclin-Dependent Kinase Inhibitor p21
• Proto-Oncogene Proteins c-bcl-2
• bcl-2-Associated X Protein
• Genistein

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis
• Cell Cycle Proteins (metabolism)
• Cell Proliferation (drug effects)
• Colonic Neoplasms (drug therapy)
• Cyclin-Dependent Kinase Inhibitor p21
• G2 Phase (drug effects)
• Genes, bcl-2 (drug effects)
• Genistein (pharmacology)
• HT29 Cells
• Humans
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• bcl-2-Associated X Protein