DNA damage response is hijacked by human papillomaviruses to complete their life cycle

The DNA damage response (DDR) is activated when DNA is altered by intrinsic or extrinsic agents. This pathway is a complex signaling network and plays important roles in genome stability, tumor transformation, and cell cycle regulation. Human papillomaviruses (HPVs) are the main etiological agents o...

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Published in:Journal of Zhejiang University. B. Science 2017-03, Vol.18 (3), p.215-232
Main Author: Hong, Shi-yuan
Format: Article
Language:English
Subjects:
Animals
Ataxia
Ataxia telangiectasia
Ataxia telangiectasia mutated protein
Ataxia Telangiectasia Mutated Proteins - genetics
Biomedical and Life Sciences
Biomedicine
Cancer
Cell Cycle
Cell Cycle Proteins - metabolism
Cell Differentiation
Cervical cancer
Cervix
death
Deoxyribonucleic acid
Deregulation
DNA
DNA Damage
DNA-Binding Proteins - metabolism
epithelium
etiological agents
Etiology
Female
Gene expression
Gene Expression Regulation, Viral
Genetic transformation
Genital tract
genome
Genome, Viral
Genomes
Human papillomavirus
Humans
Life cycle engineering
Life cycles
Mice
MicroRNAs - metabolism
Papillomaviridae
Papillomaviridae - pathogenicity
Papillomaviridae - physiology
Papillomavirus Infections - genetics
Papillomavirus Infections - virology
Review
Signal Transduction
Signaling
STAT5 Transcription Factor - genetics
Transcription
uterine cervical neoplasms
Uterine Cervical Neoplasms - virology
Viral Proteins - metabolism
Virus Replication
women
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description The DNA damage response (DDR) is activated when DNA is altered by intrinsic or extrinsic agents. This pathway is a complex signaling network and plays important roles in genome stability, tumor transformation, and cell cycle regulation. Human papillomaviruses (HPVs) are the main etiological agents of cervical cancer. Cervical cancer ranks as the fourth most common cancer among women and the second most frequent cause of cancer-related death worldwide. Over 200 types of HPVs have been identified and about one third of these infect the genital tract. The HPV life cycle is associated with epithelial differentiation. Recent studies have shown that HPVs deregulate the DDR to achieve a productive life cycle. In this review, I summarize current findings about how HPVs mediate the ataxia-telangiectasia mutated kinase (ATM) and the ATM- and RAD3-related kinase (ATR) DDRs, and focus on the roles that ATM and ATR signalings play in HPV viral replication. In addition, I demonstrate that the signal transducer and activator of transcription-5 (STAT)-5, an important immune regulator, can promote ATM and ATR activations through different mechanisms. These findings may provide novel opportunities for development of new therapeutic targets for HPV-related cancers.
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In addition, I demonstrate that the signal transducer and activator of transcription-5 (STAT)-5, an important immune regulator, can promote ATM and ATR activations through different mechanisms. 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B. Science</title><addtitle>J. Zhejiang Univ. Sci. B</addtitle><addtitle>J Zhejiang Univ Sci B</addtitle><description>The DNA damage response (DDR) is activated when DNA is altered by intrinsic or extrinsic agents. This pathway is a complex signaling network and plays important roles in genome stability, tumor transformation, and cell cycle regulation. Human papillomaviruses (HPVs) are the main etiological agents of cervical cancer. Cervical cancer ranks as the fourth most common cancer among women and the second most frequent cause of cancer-related death worldwide. Over 200 types of HPVs have been identified and about one third of these infect the genital tract. The HPV life cycle is associated with epithelial differentiation. Recent studies have shown that HPVs deregulate the DDR to achieve a productive life cycle. 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These findings may provide novel opportunities for development of new therapeutic targets for HPV-related cancers.</description><subject>Animals</subject><subject>Ataxia</subject><subject>Ataxia telangiectasia</subject><subject>Ataxia telangiectasia mutated protein</subject><subject>Ataxia Telangiectasia Mutated Proteins - genetics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer</subject><subject>Cell Cycle</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell Differentiation</subject><subject>Cervical cancer</subject><subject>Cervix</subject><subject>death</subject><subject>Deoxyribonucleic acid</subject><subject>Deregulation</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>epithelium</subject><subject>etiological agents</subject><subject>Etiology</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Viral</subject><subject>Genetic transformation</subject><subject>Genital tract</subject><subject>genome</subject><subject>Genome, Viral</subject><subject>Genomes</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Life cycle engineering</subject><subject>Life cycles</subject><subject>Mice</subject><subject>MicroRNAs - 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genetics</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer</topic><topic>Cell Cycle</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cell Differentiation</topic><topic>Cervical cancer</topic><topic>Cervix</topic><topic>death</topic><topic>Deoxyribonucleic acid</topic><topic>Deregulation</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>epithelium</topic><topic>etiological agents</topic><topic>Etiology</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Viral</topic><topic>Genetic transformation</topic><topic>Genital tract</topic><topic>genome</topic><topic>Genome, Viral</topic><topic>Genomes</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>Life cycle engineering</topic><topic>Life cycles</topic><topic>Mice</topic><topic>MicroRNAs - metabolism</topic><topic>Papillomaviridae</topic><topic>Papillomaviridae - pathogenicity</topic><topic>Papillomaviridae - 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Cervical cancer ranks as the fourth most common cancer among women and the second most frequent cause of cancer-related death worldwide. Over 200 types of HPVs have been identified and about one third of these infect the genital tract. The HPV life cycle is associated with epithelial differentiation. Recent studies have shown that HPVs deregulate the DDR to achieve a productive life cycle. In this review, I summarize current findings about how HPVs mediate the ataxia-telangiectasia mutated kinase (ATM) and the ATM- and RAD3-related kinase (ATR) DDRs, and focus on the roles that ATM and ATR signalings play in HPV viral replication. In addition, I demonstrate that the signal transducer and activator of transcription-5 (STAT)-5, an important immune regulator, can promote ATM and ATR activations through different mechanisms. These findings may provide novel opportunities for development of new therapeutic targets for HPV-related cancers.</abstract><cop>Hangzhou</cop><pub>Zhejiang University Press</pub><pmid>28271657</pmid><doi>10.1631/jzus.B1600306</doi><tpages>18</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Ataxia
Ataxia telangiectasia
Ataxia telangiectasia mutated protein
Ataxia Telangiectasia Mutated Proteins - genetics
Biomedical and Life Sciences
Biomedicine
Cancer
Cell Cycle
Cell Cycle Proteins - metabolism
Cell Differentiation
Cervical cancer
Cervix
death
Deoxyribonucleic acid
Deregulation
DNA
DNA Damage
DNA-Binding Proteins - metabolism
epithelium
etiological agents
Etiology
Female
Gene expression
Gene Expression Regulation, Viral
Genetic transformation
Genital tract
genome
Genome, Viral
Genomes
Human papillomavirus
Humans
Life cycle engineering
Life cycles
Mice
MicroRNAs - metabolism
Papillomaviridae
Papillomaviridae - pathogenicity
Papillomaviridae - physiology
Papillomavirus Infections - genetics
Papillomavirus Infections - virology
Review
Signal Transduction
Signaling
STAT5 Transcription Factor - genetics
Transcription
uterine cervical neoplasms
Uterine Cervical Neoplasms - virology
Viral Proteins - metabolism
Virus Replication
women
title DNA damage response is hijacked by human papillomaviruses to complete their life cycle
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