Inhibition of PKB/Akt activity involved in apigenin-induced apoptosis in human gastric carcinoma cel

来源 :Chinese Science Bulletin | 被引量 : 0次 | 上传用户:qq445057927
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Apigenin is a flavonoid widely distributed in fruits and vegetables. It possesses growth inhibitory properties against numerous cancer cell lines. However,the molecular mechanism(s) by which api-genin elicits its effects have not been fully elucidated. Here we studied whether apigenin inhibits growth and induces apoptosis in human gastric carcinoma cells. We showed that the flavonoid inhibited growth of the cells and caused apoptosis,as evidenced by DNA Ladder,cleavage of pro-caspase-3 in a time-dependent manner. Induction of apoptosis was dependent on inhibition of the PKB/Akt activity. We found that while apigenin had no effect on the expression of Akt and Bad,it inhibited specific phosphorylation of the two proteins that are associated with pro-survival mechanisms. We propose that this important flavonoid induces apoptosis in gastric cancer cells by inhibiting Akt activity. Since Akt is often activated in cancers,our findings may have clinical implications. It possesses growth inhibitory properties against numerous cancer cell lines. However, the molecular mechanism (s) by which api-genin elicits its effects have not been fully elucidated. Here we either selected apigenin inhibits growth and induces apoptosis in human gastric carcinoma cells. We showed that the flavonoid inhibited growth of the cells and caused apoptosis, as evidenced by DNA Ladder, cleavage of pro-caspase-3 in a time-dependent manner. Induction of apoptosis was dependent on inhibition of the PKB / Akt activity. We found that while apigenin had no effect on the expression of Akt and Bad, it inhibited specific phosphorylation of the two proteins that are associated with pro-survival mechanisms. We propose that this important flavonoid induces apoptosis in gastric cancer cells by inhibiting Akt activity. Since Akt is often activated in cancers, our findings may have clinical implications.
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