Autophagy and liver cancer

Xiaojuan Chao; Hui Qian; Shaogui Wang; Sam Fulte; Wen-Xing Ding

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자료유형: 학술저널

저자정보: Xiaojuan Chao (Department of Pharmacology Toxicology and Therapeutics University of Kansas Medical Center) Hui Qian (Department of Pharmacology Toxicology and Therapeutics University of Kansas Medical Center) Shaogui Wang (Department of Pharmacology Toxicology and Therapeutics University of Kansas Medical Center) Sam Fulte (Department of Pharmacology Toxicology and Therapeutics University of Kansas Medical Center) Wen-Xing Ding (Department of Pharmacology Toxicology and Therapeutics University of Kansas Medical Center)

저널정보: 대한간학회 Clinical and Molecular Hepatology Clinical and Molecular Hepatology 제26권 제4호

발행연도: 2020.1

수록면: 606 - 617 (12page)

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Autophagy is a highly conserved catabolic process that degrades cytosolic proteins and organelles via formation of autophagosomes that fuse with lysosomes to form autolysosomes, whereby autophagic cargos are degraded. Numerous studies have demonstrated that autophagy plays a critical role in the regulation of liver physiology and homeostasis, and impaired autophagy leads to the pathogenesis of various liver diseases such as viral hepatitis, alcohol associated liver diseases (AALD), non-alcoholic fatty liver diseases (NAFLD), and liver cancer. Recent evidence indicates that autophagy may play a dual role in liver cancer: inhibiting early tumor initiation while promoting progression and malignancy of already formed liver tumors. In this review, we summarized the progress of current understanding of how hepatic viral infection, alcohol consumption and diet-induced fatty liver diseases impair hepatic autophagy. We also discussed how impaired autophagy promotes liver tumorigenesis, and paradoxically how autophagy is required to promote the malignancy and progression of liver cancer. Understanding the molecular mechanisms underlying how autophagy differentially affects liver cancer development and progression may help to design better therapeutic strategies for prevention and treatment of liver cancer.

#Alcohol #mTOR #Nrf2 #p62 #TFEB

참고문헌 (55)

참고문헌 신청

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Katsuragi Y / 2016 / Regulation of the Keap1–Nrf2pathway by p62/SQSTM1 / Curr Opin Toxicol 1:54~61

Komatsu M / 2010 / The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1 / Nat Cell Biol 12:213~223

Ichimura Y / 2013 / Phosphorylation of p62 activates the Keap1-Nrf2 pathway during selective autophagy / Mol Cell 51:618~631

Jain A / 2010 / p62/SQSTM1 is a target gene for transcription factor NRF2 and creates a positive feedback loop by inducing antioxidant response element-driven gene transcription / J Biol Chem 285:22576~22591

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