Bcl-xL Blocks Transforming Growth Factor-β1-induced Apoptosis by Inhibiting Cytochrome c Release and Not by Directly Antagonizing Apaf-1-dependent Caspase Activation in Prostate Epithelial Cells
作者： Jerry E Chipuk , Manjunatha Bhat , Andrew Y Hsing , Jianjie Ma , David Danielpour
关键词: Transforming growth factor 、 Bcl-xL 、 Intrinsic apoptosis 、 Cell biology 、 Biology 、 Apoptosis 、 Cytochrome c 、 Caspase 、 Molecular biology 、 Poly ADP ribose polymerase 、 Cytochrome
摘要: Abstract The mechanism by which transforming growth factor-β1 (TGF-β1) induces apoptosis of prostate epithelial cells was studied in the NRP-154 rat cell line. TGF-β1 down-regulates expression Bcl-xL and poly(ADP-ribosyl)polymerase (PARP), promotes cytochrome crelease, up-regulates latent caspase-3, activates caspases 3 9. We tested role this cascade stably overexpressing to prevent loss TGF-β1. Clones are resistant with respect induction apoptosis, c release, activation 9 3, cleavage PARP; yet they remain sensitive cycle arrest, both fibronectin caspase-3 expression, PARP expression. show that associates Apaf-1 cells; but association does not inhibit c. Together, our data suggest through Bcl-xL, leading release subsequent 3. Moreover, demonstrate antiapoptotic effect occurs inhibition mitochondrial antagonizing Apaf-1-dependent processing
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