Link to the University of Pittsburgh Homepage
Link to the University Library System Homepage Link to the Contact Us Form

Autophagy: Dual Response in the Development of Hepatocellular Carcinoma

Yazdani, Hamza and Huang, Hai and Tsung, Allan (2019) Autophagy: Dual Response in the Development of Hepatocellular Carcinoma. Cells, 8 (2). p. 91. ISSN 2073-4409 (Submitted)

Published Version

Download (683kB) | Preview


Autophagy is an evolutionary conserved intracellular mechanism which helps eukaryotic cells in maintaining their metabolic state to afford high-efficiency energy requirements. In the physiology of a normal liver and the pathogenesis of liver diseases, autophagy plays a crucial role. Autophagy has been found to be both upregulated and downregulated in different cancers providing the evidence that autophagy plays a dual role in suppressing and promoting cell survival. Hepatocellular carcinoma (HCC) is the most common primary liver cancer and the major leading cause of cancer mortality worldwide. In light of its high complexity and poor prognosis, it is essential to improve our understanding of autophagy’s role in HCC. In this review, we summarize the dual mechanism of autophagy in the development of HCC and elucidate the currently used therapeutic strategies for anti-HCC therapy


Social Networking:
Share |


Item Type: Article
Status: Submitted
CreatorsEmailPitt UsernameORCID
Yazdani, Hamzahoy20@pitt.eduhoy20
Huang, Hai
Tsung, Allan
Date: 28 January 2019
Date Type: Publication
Journal or Publication Title: Cells
Volume: 8
Number: 2
Publisher: MDPI AG
Page Range: p. 91
DOI or Unique Handle: 10.3390/cells8020091
Schools and Programs: School of Medicine > Surgery
Refereed: Yes
Uncontrolled Keywords: hepatocellular carcinoma, inflammation, mitophagy, oxidative stress, HCC therapy
ISSN: 2073-4409
Official URL:
Funders: National Institute of Health
Article Type: Review
Date Deposited: 29 Jun 2021 18:47
Last Modified: 29 Jun 2021 18:47


Monthly Views for the past 3 years

Plum Analytics

Actions (login required)

View Item View Item