XXXX Cdelta amplifies @entity2367 formation via mitochondrial signaling in @entity263 cells.

@entity263 @entity4674 @entity12703 @entity16084 @entity1311 @entity8187 @entity2879 @entity29682 @entity2367 @entity4456 @entity24399 @entity4291
We studied the role of @entity16084 C isoform @entity4456 in @entity2367 ( @entity24399 ) formation, as well as in the mitochondrial apoptosis pathway induced by anticancer drugs in @entity263 ( @entity263 ) cells. @entity2879 and @entity1311 induced @entity24399 formation and apoptosis in @entity4456 -positive LNCaP and DU145 cells but not in @entity4456 -negative LN-TPA or @entity263 -3 cells. In contrast, these drugs induced mitotic cell cycle arrest in all @entity263 cell lines. Treatment with @entity12703 , a specific @entity4456 inhibitor, significantly inhibited drug-induced @entity24399 formation and apoptosis in LNCaP cells, as did overexpression of dominant negative-type @entity4456 . Overexpression of wild-type @entity4456 had an opposite effect in @entity263 -3 cells. Notably, @entity2879 induced biphasic @entity24399 formation in LNCaP cells. The early and transient @entity24399 increase resulted from de novo @entity24399 synthesis, while the late and sustained @entity24399 accumulation was derived from @entity4291 hydrolysis by @entity29682 ( @entity29682 ). @entity24399 , in turn, induced mitochondrial translocation of @entity4456 and stimulated the activity of this kinase, promoting @entity4674 release and @entity8187 activation. Furthermore, the specific @entity8187 inhibitor LEHD-fmk significantly inhibited @entity2879 -induced @entity29682 activation, @entity24399 accumulation, and @entity4456 mitochondrial translocation. These results indicate that @entity4456 plays a crucial role in activating anticancer drug-induced apoptosis signaling by amplifying the @entity24399 -mediated mitochondrial amplification loop.
