Autophagy plays an important role in the healthy and diseased liver. The aim of this investigation is to evaluate molecular mechanisms of autophagy in liver diseases especially HCC.

by searching PUBMED and Scopus DATA base from 2012 to 2017.

In HCC, autophagy level would be reduced and provoking autophagy as an antitumor mechanism could have beneficial effect in patients with HCC. HGF/c-MET signaling suppresses autophagy via interaction with PI3K/AKT pathway while overexpression of c-MET was observed in HCC samples. By promotion or inhibition of autophagy, these pathways affect the development of HCC. The anti-necrotic function of autophagy is critical for tumorigenesis of many tumor cells, including hepatocellular carcinoma (HCC). Inhibitors of autophagy such as 3-MA (3-methyladenine) which blocks the fusion between autophagosome and lysosome can enhance pro-apoptotic effects of meloxicam in HCC cells. Autophagy inhibitors have been used to enhance the sensitivity of various cancers toward chemotherapy. Under cellular stress conditions, such as nutrient deficiency, chemotherapy and or radiotherapy, autophagy is rapidly activated to maintain the survival of tumor cells. Therefore, autophagy has been proposed as a potential mechanism of cancer drug resistance. Among the many factors, therapy-induced autophagy represents a novel mechanism of resistance to anticancer therapy.

Accumulating evidence shows that modulating the level of autophagy may be useful as a therapeutic strategy to enhance the efficacy of many antitumor agents, including cisplatin, Dox and sorafenib in HCC.