Macroautophagy modulates cellular response to proteasome inhibitors in cancer therapy
Publication in refereed journal


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摘要Macroautophagy 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.
著者Wu WKK, Sakamoto KM, Milani M, Aldana-Masankgay G, Fan DM, Wu KC, Lee CW, Cho CH, Yu J, Sung JJY
期刊名稱Drug Resistance Updates
出版年份2010
月份6
日期1
卷號13
期次3
出版社CHURCHILL LIVINGSTONE
頁次87 - 92
國際標準期刊號1368-7646
語言英式英語
關鍵詞Aggresome; ATF4; Bortezomib; HDAC6; IRE1-JNK; LC3; mTOR
Web of Science 學科類別Pharmacology & Pharmacy; PHARMACOLOGY & PHARMACY

上次更新時間 2021-25-01 於 02:20