ABSTRACT
OBJECTIVE: The study is to explore the effects of genistein on proliferation and apoptosis in human colon cancer HT-29 cells and the likely underlying molecular mechanisms. METHODS: HT-29 cultures were maintained in DMEM containing 10% fetal bovine serum. Cell proliferation was determined by MTT assay and cell cycle distribution by cytometry. Apoptosis was detected by the Cell Death Detection ELISA and cytometry. The expressions of bax, bcl-2, and PCNA were examined using reverse transcriptase-polymerase chain reaction (RT-PCR) and Western-blot both at mRNA and protein levels, respectively. RESULTS: Genistein inhibited proliferation and induced G2/M phase arrest and apoptotic death in colon cancer HT-29 cells. We investigated the effects of genistein on molecules that regulate apoptosis and cell cycle progress. Genistein increased expression of bax and significantly reduced PCNA with a slightly decrease in bcl-2 expression both at mRNA and protein level. CONCLUSION: Our results demonstrated that genistein inhibited the viability of human colon cancer HT-29 cell via induction of apoptosis mainly through regulation of PCNA and Bax/Bcl-2 expression. These data suggested a role of genistein in prevention of colon tumor and might reduce colon tumor growth.
Subject(s)
Anticarcinogenic Agents/pharmacology , Apoptosis/drug effects , Cell Proliferation/drug effects , Genistein/pharmacology , HT29 Cells , Humans , Phytoestrogens/pharmacology , Proliferating Cell Nuclear Antigen/genetics , Proliferating Cell Nuclear Antigen/metabolism , Proto-Oncogene Proteins c-bcl-2/genetics , Proto-Oncogene Proteins c-bcl-2/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolismABSTRACT
OBJECTIVE: The aim of this investigation was to study the effects of fat-soluble extracts from vegetable powder (FEFVP) and beta-carotene on the proliferation and apoptosis of cultured YTMLC-90 lung cancer cells. METHODS: The lung cancer cells were continuously exposed to a broad range of concentration of FEFVP and beta-carotene. The proliferation was evaluated in MTT test. The induction of apoptosis was evaluated by morphological change, DNA fragmentation analysis, and DNA content analysis combined with flow cytometric analysis. RESULTS: Both FEFVP and beta-carotene were found to inhibit cell proliferation and to induce morphologic changes consistent with apoptosis in YTMLC-90 cancer cells, including cellular shrinkage, chromatin condensation and nuclear fragmentation. DNA agarose gel electrophoresis showed DNA fragmentation 'ladder'. Flow cytometric analysis revealed decreased DNA content and the presence of a sub-G1 apoptotic peak. CONCLUSION: These findings are consistent with the induction of apoptosis. Moreover, the effects of FEFVP are stronger than those of beta-carotene. FEFVP inhibits the growth of YTMLC-90 probably via the induction of apoptosis cancer cells.