MYC activity mitigates response to rapamycin in prostate cancer through 4EBP1-mediated inhibition of autophagy

 Abstract

Cancer cells have evolved exquisitely to ignore both intrinsic and extrinsic cell death signals, and resistance to cell death is a critical challenge facing clinical oncology. Autophagy, the catabolic recycling process that involves the fusion of autophagosomes containing sequestered cargo with lysosomes, has an enigmatic role in tumorigenesis. In times of metabolic stress due to deprived nutrition or hypoxia, tumor cells use autophagy as a scavenging mechanism for maintenance of critical processes and survival. However, modulation of the extent of autophagy plays a critical role, as excessive autophagy can result in a non-apoptotic and non-necrotic cell death (sometimes referred to as Type II programmed cell death). It is likely that the genetic context of specific cancers will have an impact upon whether autophagy is primarily a mechanism for survival or cell death.

 Related Article:

ZB Ding, YH Shi, J Zhou, SJ Qiu, Y Xu, Z Dai, GM Shi, XY Wang, AW Ke, B Wu, J Fan. Association of autophagy defect with a malignant phenotype and poor prognosis of hepatocellular carcinoma. Cancer Res 2008; 68: 9167- 75.
PMID: 21199803 DOI: 10.1158/0008-5472.CA

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Pages
281 - 282
doi
10.4161/auto.6.2.10921
Type
Autophagic Punctum
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MYC activity mitigates response to rapamycin in prostate cancer through 4EBP1-mediated inhibition of autophagy