Chaperone-mediated autophagy substrate proteins in cancer
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Ying Tang1,*, Xiong-Wen Wang1,*, Zhan-Hua Liu1, Yun-Ming Sun2, Yu-Xin Tang2 and Dai-Han Zhou1
1Department of Oncology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, China
2Department of Gynecology and Obstetrics, Maternal and Child Health Hospital of Zhoushan, Zhoushan 316000, China
*These authors have contributed equally to this work
Dai-Han Zhou, email: firstname.lastname@example.org
Yu-Xin Tang, email: email@example.com
Keywords: chaperone-mediated autophagy, substrate proteins, cancer, glycolysis, Warburg effect
Received: January 09, 2017 Accepted: April 07, 2017 Published: May 03, 2017
All intracellular proteins undergo continuous synthesis and degradation. Chaperone-mediated autophagy (CMA) is necessary to maintain cellular homeostasis through turnover of cytosolic proteins (substrate proteins). This degradation involves a series of substrate proteins including both cancer promoters and suppressors. Since activating or inhibiting CMA pathway to treat cancer is still debated, targeting to the CMA substrate proteins provides a novel direction. We summarize the cancer-associated substrate proteins which are degraded by CMA. Consequently, CMA substrate proteins catalyze the glycolysis which contributes to the Warburg effect in cancer cells. The fact that the degradation of substrate proteins based on the CMA can be altered by posttranslational modifications such as phosphorylation or acetylation. In conclusion, targeting to CMA substrate proteins develops into a new anticancer therapeutic approach.
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