Обзорная статья

Role of regulatory miRNAs of the PI3K/AKT/mTOR signaling in the pathogenesis of hepatocellular carcinoma

Farzad RahmaniDepartment of Clinical Biochemistry, Faculty of Medicine Mashhad University of Medical Sciences Mashhad IranAghigh ZiaeemehrSurgical Oncology Research Center Mashhad University of Medical Sciences Mashhad IranSoodabeh ShahidsalesCancer Research Center Mashhad University of Medical Sciences Mashhad IranMasoumeh GharibDepartment of Pathology, Faculty of Medicine Mashhad University of Medical Sciences Mashhad IranMajid KhazaeiDepartment of Medical Physiology, Faculty of Medicine Mashhad University of Medical Sciences Mashhad IranGordon A. FernsDivision of Medical Education Brighton and Sussex Medical School Brighton UKMikhail RyzhikovDivision of Pulmonary and Critical Care Medicine, School of Medicine Washington University Saint Louis MissouriAmir AvanDepartment of Modern Sciences and Technologies, Faculty of Medicine Mashhad University of Medical Sciences Mashhad IranSeyed Mahdi HassanianDepartment of Clinical Biochemistry, Faculty of Medicine Mashhad University of Medical Sciences Mashhad Iran

2019en

ABI

Аннотация

Hepatocellular carcinoma (HCC) is one of the common malignant human tumors with high morbidity worldwide. Aberrant activation of the oncogenic phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling is related to clinicopathological features of HCC. Emerging data revealed that microRNAs (miRNAs) have prominent implications for regulating cellular proliferation, differentiation, apoptosis, and metabolism through targeting the PI3K/AKT/mTOR signaling axis. The recognition of the crucial role of miRNAs in hepatocarcinogenesis represents a promising area to identify novel anticancer therapeutics for HCC. The present study summarizes the major findings about the regulatory role of miRNAs in the PI3K/AKT/mTOR pathway in the pathogenesis of HCC.

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Идентификаторы

DOI: 10.1002/jcp.29333

Цитирования и источники

Цитирований: 3Использованных источников: 0

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