Oncotarget

Reviews:

Chaperonemediated 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

Correspondence to:

Dai-Han Zhou, email: 13902206571@139.com

Yu-Xin Tang, email: yingying19870722@163.com

Keywords: chaperone-mediated autophagy, substrate proteins, cancer, glycolysis, Warburg effect

Received: January 09, 2017     Accepted: April 07, 2017     Published: May 03, 2017

ABSTRACT

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.