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Cancer Lett. 2011 Mar 1;302(1):29-36. doi: 10.1016/j.canlet.2010.12.007. Epub 2011 Jan 8.

Induction of autophagy-dependent apoptosis by the survivin suppressant YM155 in prostate cancer cells.

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Research Institute of Oncology, People's Liberty Army, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.


In this study, we demonstrated that YM155, a novel survivin suppressant, induced both apoptosis, and autophagy that was shown by conversion of cytosolic-associated protein light chain 3 (LC3I) into autophagosome-associated form (LC3II) and a punctate fluorescence pattern of an ectopic GFP-LC3 protein. The lysosomal inhibitor chloroquine further accumulated YM155-induced LC3II, indicating an increase of autophagic flux. Ectopic expression of survivin significantly attenuated YM155-induced apoptosis and autophagy, whereas survivin siRNA induced autophagy. Furthermore, inhibition of either early or late events of autophagy attenuated YM155-induced apoptosis, demonstrating that induction of autophagy proceeds apoptosis. In conclusion, suppression of survivin by YM155 induces autophagy-dependent apoptosis, and YM155-induced autophagy plays a pro-apoptotic role thereby unveiling a novel mechanism of YM155 in prostate cancer cells.

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