Links between Human LINE-1 Retrotransposons and Hepatitis Virus-Related Hepatocellular Carcinoma
Hepatocellular carcinoma (HCC) accounts for approximately 80% of liver cancers, the third most frequent cause of cancer mortality. The most prevalent risk factors for HCC are infections by hepatitis B or hepatitis C virus. Findings suggest that hepatitis virus-related HCC might be a cancer in which...
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pubmed-48636592016-05-30 Links between Human LINE-1 Retrotransposons and Hepatitis Virus-Related Hepatocellular Carcinoma Honda, Tomoyuki Chemistry Hepatocellular carcinoma (HCC) accounts for approximately 80% of liver cancers, the third most frequent cause of cancer mortality. The most prevalent risk factors for HCC are infections by hepatitis B or hepatitis C virus. Findings suggest that hepatitis virus-related HCC might be a cancer in which LINE-1 retrotransposon, often termed L1, activity plays a potential role. Firstly, hepatitis viruses can suppress host defense factors that also control L1 mobilization. Secondly, many recent studies also have indicated that hypomethylation of L1 affects the prognosis of HCC patients. Thirdly, endogenous L1 retrotransposition was demonstrated to activate oncogenic pathways in HCC. Fourthly, several L1 chimeric transcripts with host or viral genes are found in hepatitis virus-related HCC. Such lines of evidence suggest a linkage between L1 retrotransposons and hepatitis virus-related HCC. Here, I briefly summarize current understandings of the association between hepatitis virus-related HCC and L1. Then, I discuss potential mechanisms of how hepatitis viruses drive the development of HCC via L1 retrotransposons. An increased understanding of the contribution of L1 to hepatitis virus-related HCC may provide unique insights related to the development of novel therapeutics for this disease. Frontiers Media S.A. 2016-05-11 /pmc/articles/PMC4863659/ /pubmed/27242996 http://dx.doi.org/10.3389/fchem.2016.00021 Text en Copyright © 2016 Honda. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Honda, Tomoyuki |
spellingShingle |
Honda, Tomoyuki Links between Human LINE-1 Retrotransposons and Hepatitis Virus-Related Hepatocellular Carcinoma |
author_facet |
Honda, Tomoyuki |
author_sort |
Honda, Tomoyuki |
title |
Links between Human LINE-1 Retrotransposons and Hepatitis Virus-Related Hepatocellular Carcinoma |
title_short |
Links between Human LINE-1 Retrotransposons and Hepatitis Virus-Related Hepatocellular Carcinoma |
title_full |
Links between Human LINE-1 Retrotransposons and Hepatitis Virus-Related Hepatocellular Carcinoma |
title_fullStr |
Links between Human LINE-1 Retrotransposons and Hepatitis Virus-Related Hepatocellular Carcinoma |
title_full_unstemmed |
Links between Human LINE-1 Retrotransposons and Hepatitis Virus-Related Hepatocellular Carcinoma |
title_sort |
links between human line-1 retrotransposons and hepatitis virus-related hepatocellular carcinoma |
description |
Hepatocellular carcinoma (HCC) accounts for approximately 80% of liver cancers, the third most frequent cause of cancer mortality. The most prevalent risk factors for HCC are infections by hepatitis B or hepatitis C virus. Findings suggest that hepatitis virus-related HCC might be a cancer in which LINE-1 retrotransposon, often termed L1, activity plays a potential role. Firstly, hepatitis viruses can suppress host defense factors that also control L1 mobilization. Secondly, many recent studies also have indicated that hypomethylation of L1 affects the prognosis of HCC patients. Thirdly, endogenous L1 retrotransposition was demonstrated to activate oncogenic pathways in HCC. Fourthly, several L1 chimeric transcripts with host or viral genes are found in hepatitis virus-related HCC. Such lines of evidence suggest a linkage between L1 retrotransposons and hepatitis virus-related HCC. Here, I briefly summarize current understandings of the association between hepatitis virus-related HCC and L1. Then, I discuss potential mechanisms of how hepatitis viruses drive the development of HCC via L1 retrotransposons. An increased understanding of the contribution of L1 to hepatitis virus-related HCC may provide unique insights related to the development of novel therapeutics for this disease. |
publisher |
Frontiers Media S.A. |
publishDate |
2016 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4863659/ |
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1613578046313332736 |