XXXX induces cell apoptosis of @entity1 @entity511 cells through @entity25087 pathway.

@entity3978 @entity1 @entity511 @entity589 @entity2428 @entity588 @entity3478 @entity5 @entity1836 @entity26 @entity25087 @entity3089 @entity3090 @entity4675 @entity1435
@entity511 is a @entity3478 that responds poorly to both chemotherapy and radiation therapy. @entity3089 ( @entity3090 ), the major @entity3978 in green tea, has been shown to inhibit tumorigenesis and @entity5 cell growth in animal models. The aim of this study was to elucidate the mechanism of @entity3090 -induced apoptosis of @entity1 @entity511 cells. @entity3090 induced cell apoptosis in @entity1 @entity511 cell lines but not primary chondrocytes. @entity3090 induced upregulation of @entity589 and @entity2428 , downregulation of @entity588 and @entity1836 , and dysfunction of mitochondria in @entity511 . We also found that the accumulation of reactive @entity26 species (ROS) is a critical mediator in @entity3090 -induced cell death. @entity3090 induced @entity25087 ( @entity25087 ) dephosphorylation and its dissociation from 14-3-3. Treatment of @entity511 cells with @entity3090 induced @entity1435 and @entity4675 ( @entity4675 ) phosphorylation. Transfection with @entity25087 siRNA or @entity1435 and @entity4675 mutant antagonized the @entity3090 -induced cell apoptosis. Therefore, @entity3090 triggered ROS and activated the @entity25087 - @entity1435 / @entity4675 pathway, resulting @entity511 cell death. Importantly, animal studies revealed a dramatic reduction in @entity5 volume after 24 days of treatment. Thus, @entity3090 may be a novel anti- @entity5 agent for the treatment of @entity511 .
