Author:
Hashemi Mehrdad,Nadafzadeh Niloufar,Imani Mohammad Hassan,Rajabi Romina,Ziaolhagh Setayesh,Bayanzadeh Seyedeh Delaram,Norouzi Raheleh,Rafiei Reihaneh,Koohpar Zeinab Khazaei,Raei Behnaz,Zandieh Mohammad Arad,Salimimoghadam Shokooh,Entezari Maliheh,Taheriazam Afshin,Alexiou Athanasios,Papadakis Marios,Tan Shing Cheng
Abstract
AbstractAutophagy is an evolutionarily conserved process that plays a role in regulating homeostasis under physiological conditions. However, dysregulation of autophagy is observed in the development of human diseases, especially cancer. Autophagy has reciprocal functions in cancer and may be responsible for either survival or death. Hepatocellular carcinoma (HCC) is one of the most lethal and common malignancies of the liver, and smoking, infection, and alcohol consumption can lead to its development. Genetic mutations and alterations in molecular processes can exacerbate the progression of HCC. The function of autophagy in HCC is controversial and may be both tumor suppressive and tumor promoting. Activation of autophagy may affect apoptosis in HCC and is a regulator of proliferation and glucose metabolism. Induction of autophagy may promote tumor metastasis via induction of EMT. In addition, autophagy is a regulator of stem cell formation in HCC, and pro-survival autophagy leads to cancer cell resistance to chemotherapy and radiotherapy. Targeting autophagy impairs growth and metastasis in HCC and improves tumor cell response to therapy. Of note, a large number of signaling pathways such as STAT3, Wnt, miRNAs, lncRNAs, and circRNAs regulate autophagy in HCC. Moreover, regulation of autophagy (induction or inhibition) by antitumor agents could be suggested for effective treatment of HCC. In this paper, we comprehensively review the role and mechanisms of autophagy in HCC and discuss the potential benefit of targeting this process in the treatment of the cancer.
Graphical abstract
Funder
Projekt Deal
Ministry of Higher Education, Malaysia
Universiti Kebangsaan Malaysia
Private Universität Witten/Herdecke gGmbH
Publisher
Springer Science and Business Media LLC
Subject
Cell Biology,Molecular Biology,Biochemistry
Cited by
23 articles.
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