HERVs and Cancer—A Comprehensive Review of the Relationship of Human Endogenous Retroviruses and Human Cancers

Genomic instability and genetic mutations can lead to exhibition of several cancer hallmarks in affected cells such as sustained proliferative signaling, evasion of growth suppression, activated invasion, deregulation of cellular energetics, and avoidance of immune destruction. Similar biological ch...

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Main Authors: Erik Stricker, Erin C. Peckham-Gregory, Michael E. Scheurer
Format: Article
Language:English
Published: MDPI AG 2023-03-01
Series:Biomedicines
Subjects:
Online Access:https://www.mdpi.com/2227-9059/11/3/936
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author Erik Stricker
Erin C. Peckham-Gregory
Michael E. Scheurer
author_facet Erik Stricker
Erin C. Peckham-Gregory
Michael E. Scheurer
author_sort Erik Stricker
collection DOAJ
description Genomic instability and genetic mutations can lead to exhibition of several cancer hallmarks in affected cells such as sustained proliferative signaling, evasion of growth suppression, activated invasion, deregulation of cellular energetics, and avoidance of immune destruction. Similar biological changes have been observed to be a result of pathogenic viruses and, in some cases, have been linked to virus-induced cancers. Human endogenous retroviruses (HERVs), once external pathogens, now occupy more than 8% of the human genome, representing the merge of genomic and external factors. In this review, we outline all reported effects of HERVs on cancer development and discuss the HERV targets most suitable for cancer treatments as well as ongoing clinical trials for HERV-targeting drugs. We reviewed all currently available reports of the effects of HERVs on human cancers including solid tumors, lymphomas, and leukemias. Our review highlights the central roles of HERV genes, such as <i>gag</i>, <i>env</i>, <i>pol</i>, <i>np9</i>, and <i>rec</i> in immune regulation, checkpoint blockade, cell differentiation, cell fusion, proliferation, metastasis, and cell transformation. In addition, we summarize the involvement of HERV long terminal repeat (LTR) regions in transcriptional regulation, creation of fusion proteins, expression of long non-coding RNAs (lncRNAs), and promotion of genome instability through recombination.
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spelling doaj.art-48309007210849aaa1fd6869845c4aa92023-11-17T09:47:46ZengMDPI AGBiomedicines2227-90592023-03-0111393610.3390/biomedicines11030936HERVs and Cancer—A Comprehensive Review of the Relationship of Human Endogenous Retroviruses and Human CancersErik Stricker0Erin C. Peckham-Gregory1Michael E. Scheurer2Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77047, USADepartment of Pediatrics, Baylor College of Medicine, Houston, TX 77047, USADepartment of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77047, USAGenomic instability and genetic mutations can lead to exhibition of several cancer hallmarks in affected cells such as sustained proliferative signaling, evasion of growth suppression, activated invasion, deregulation of cellular energetics, and avoidance of immune destruction. Similar biological changes have been observed to be a result of pathogenic viruses and, in some cases, have been linked to virus-induced cancers. Human endogenous retroviruses (HERVs), once external pathogens, now occupy more than 8% of the human genome, representing the merge of genomic and external factors. In this review, we outline all reported effects of HERVs on cancer development and discuss the HERV targets most suitable for cancer treatments as well as ongoing clinical trials for HERV-targeting drugs. We reviewed all currently available reports of the effects of HERVs on human cancers including solid tumors, lymphomas, and leukemias. Our review highlights the central roles of HERV genes, such as <i>gag</i>, <i>env</i>, <i>pol</i>, <i>np9</i>, and <i>rec</i> in immune regulation, checkpoint blockade, cell differentiation, cell fusion, proliferation, metastasis, and cell transformation. In addition, we summarize the involvement of HERV long terminal repeat (LTR) regions in transcriptional regulation, creation of fusion proteins, expression of long non-coding RNAs (lncRNAs), and promotion of genome instability through recombination.https://www.mdpi.com/2227-9059/11/3/936human endogenous retrovirusbreast cancerleukemialymphomaskin cancerreproductive cancer
spellingShingle Erik Stricker
Erin C. Peckham-Gregory
Michael E. Scheurer
HERVs and Cancer—A Comprehensive Review of the Relationship of Human Endogenous Retroviruses and Human Cancers
Biomedicines
human endogenous retrovirus
breast cancer
leukemia
lymphoma
skin cancer
reproductive cancer
title HERVs and Cancer—A Comprehensive Review of the Relationship of Human Endogenous Retroviruses and Human Cancers
title_full HERVs and Cancer—A Comprehensive Review of the Relationship of Human Endogenous Retroviruses and Human Cancers
title_fullStr HERVs and Cancer—A Comprehensive Review of the Relationship of Human Endogenous Retroviruses and Human Cancers
title_full_unstemmed HERVs and Cancer—A Comprehensive Review of the Relationship of Human Endogenous Retroviruses and Human Cancers
title_short HERVs and Cancer—A Comprehensive Review of the Relationship of Human Endogenous Retroviruses and Human Cancers
title_sort hervs and cancer a comprehensive review of the relationship of human endogenous retroviruses and human cancers
topic human endogenous retrovirus
breast cancer
leukemia
lymphoma
skin cancer
reproductive cancer
url https://www.mdpi.com/2227-9059/11/3/936
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