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Autophagy: Dual Response in the Development of Hepatocellular Carcinoma
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 be...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6406383/ https://www.ncbi.nlm.nih.gov/pubmed/30695997 http://dx.doi.org/10.3390/cells8020091 |
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author | Yazdani, Hamza O. Huang, Hai Tsung, Allan |
author_facet | Yazdani, Hamza O. Huang, Hai Tsung, Allan |
author_sort | Yazdani, Hamza O. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6406383 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-64063832019-03-19 Autophagy: Dual Response in the Development of Hepatocellular Carcinoma Yazdani, Hamza O. Huang, Hai Tsung, Allan Cells Review 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. MDPI 2019-01-28 /pmc/articles/PMC6406383/ /pubmed/30695997 http://dx.doi.org/10.3390/cells8020091 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Yazdani, Hamza O. Huang, Hai Tsung, Allan Autophagy: Dual Response in the Development of Hepatocellular Carcinoma |
title | Autophagy: Dual Response in the Development of Hepatocellular Carcinoma |
title_full | Autophagy: Dual Response in the Development of Hepatocellular Carcinoma |
title_fullStr | Autophagy: Dual Response in the Development of Hepatocellular Carcinoma |
title_full_unstemmed | Autophagy: Dual Response in the Development of Hepatocellular Carcinoma |
title_short | Autophagy: Dual Response in the Development of Hepatocellular Carcinoma |
title_sort | autophagy: dual response in the development of hepatocellular carcinoma |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6406383/ https://www.ncbi.nlm.nih.gov/pubmed/30695997 http://dx.doi.org/10.3390/cells8020091 |
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