Induction of cell cycle arrest and apoptosis in @entity1 XXXX cells by @entity3092 .

@entity1 @entity10610 @entity0 @entity5 @entity8189 @entity876 @entity3092 @entity994
@entity3092 , a widely distributed bioflavonoid, has been shown to induce growth inhibition in certain @entity5 cell types. In the present study we have pursued the mechanism of growth inhibition in MCF-7 @entity1 @entity0 cells. @entity3092 treatment resulted in the accumulation of cells specifically at G2/M phase of the cell cycle. Mitotic index measured by MPM2 staining clearly showed that cells were transiently accumulated in M phase, 24 h after treatment. The transient M phase accumulation was accompanied by a transient increase in the levels of @entity8189 and @entity10610 kinase activity. However, 24 h or longer treatment caused a marked accumulation of cells in G2 instead of M phase. Levels of @entity8189 and @entity8189 -associated @entity10610 kinase activity were also decreased. We also found that @entity3092 markedly increased Cdk-inhibitor @entity994 / @entity994 protein level after treatment for 48 h or longer, and the induction of @entity994 / @entity994 increased its association with @entity10610 - @entity8189 complex, however, up-regulation of @entity876 by @entity3092 was not observed. @entity3092 also induced significant apoptosis in MCF-7 cells in addition to cell cycle arrest, and the induction of apoptosis was markedly blocked by antisense @entity994 / @entity994 expression. The present data, therefore, demonstrate that a flavonoid @entity3092 induces growth inhibition in the @entity1 @entity0 cell line MCF-7 through at least two different mechanisms; by inhibiting cell cycle progression through transient M phase accumulation and subsequent G2 arrest, and by inducing apoptosis.
