Macroautophagy modulates cellular response to proteasome inhibitors in cancer therapy
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AbstractMacroautophagy and the ubiquitin-proteasome system are two complementary pathways for protein degradation. The former degrades long-lived proteins and damaged organelles while the later degrades short-lived proteins. Recent findings indicate that suppression of the ubiquitin-proteasome system by proteasome inhibitors induces macroautophagy through multiple pathways, including) accumulation of ubiquitinated proteins and activation of HDAC6; (2) activation of the IRE1-JNK pathway; (3) proteasomal stabilization of ATF4; (4) inhibition of mTOR complex 1 signaling; (5) reduced proteasomal degradation of LC3. Induction of macroautophagy attenuates the antitumor effect of proteasome inhibitors in various types of cancer. These findings suggest that inhibition of macroautophagy may represent a novel strategy to enhance cellular sensitivity to proteasome inhibition. (C) 2010 Elsevier Ltd. All rights reserved.
All Author(s) ListWu WKK, Sakamoto KM, Milani M, Aldana-Masankgay G, Fan DM, Wu KC, Lee CW, Cho CH, Yu J, Sung JJY
Journal nameDrug Resistance Updates
Year2010
Month6
Day1
Volume Number13
Issue Number3
PublisherCHURCHILL LIVINGSTONE
Pages87 - 92
ISSN1368-7646
LanguagesEnglish-United Kingdom
KeywordsAggresome; ATF4; Bortezomib; HDAC6; IRE1-JNK; LC3; mTOR
Web of Science Subject CategoriesPharmacology & Pharmacy; PHARMACOLOGY & PHARMACY

Last updated on 2020-18-10 at 01:43