A new anticancer compound, @entity59760 , inhibits @entity5 growth and promotes apoptosis in HeLa cells through XXXX activation.

@entity1 @entity1262 @entity137 @entity589 @entity522 @entity1722 @entity5 @entity19 @entity4674 @entity1836 @entity1311 @entity8186 @entity2879 @entity59760 @entity5713
@entity59760 (OC) was identified as a potent apoptosis inducer from an herbal plant, Garcinia yunnanensis, during our previous bioassay-guided drug screening. In this study, we investigated the signaling pathways through which OC activated apoptosis in HeLa cells. We also compared the IC(50) values of OC with that of @entity2879 , @entity1311 and @entity5713 in @entity5 cell lines including @entity1722 and @entity1262 overexpressing cells. In addition, the in vivo antitumor effect of OC was studied in @entity19 model. Our results showed that OC induced a caspase-dependent apoptosis by triggering a series of events in HeLa cells including @entity589 translocation, @entity4674 release, @entity522 activation, chromosome fragmentation followed by @entity8186 activation, Bid cleavage and eventually cell death. Addition of a pan-caspase inhibitor or overexpression of an anti-apoptotic protein, @entity1836 , prevented OC-induced cell death. Moreover, OC exhibited a wide anticancer spectrum in @entity5 cell lines with comparable IC(50) values, regardless of the expression levels of @entity1722 and @entity1262 . In contrast, the IC(50) values of three clinical anticancer drugs, @entity2879 , @entity1311 and @entity5713 were significantly elevated in @entity1722 and/or @entity1262 overexpressing cells. Furthermore, OC showed a similar antitumor effect but lower general @entity137 than @entity2879 against xenografted @entity1 @entity5 in @entity19 model. All these data suggested that OC is a promising apoptosis inducer with the potential to be developed into a clinical anticancer drug.
