GlutaredoxinV1, Main, Exploration, bibRecord, 000011

TRIAP1 knockdown sensitizes non-small cell lung cancer to ionizing radiation by disrupting redox homeostasis.

Identifieur interne : 000011 ( Main/Exploration ); précédent : 000010; suivant : 000012

TRIAP1 knockdown sensitizes non-small cell lung cancer to ionizing radiation by disrupting redox homeostasis.

Auteurs : Chun-Cheng Hao [République populaire de Chine] ; Jia-Ning Luo [République populaire de Chine] ; Cui-Yang Xu [République populaire de Chine] ; Xin-Yu Zhao [République populaire de Chine] ; Zhen-Bin Zhong [République populaire de Chine] ; Xiao-Nan Hu [République populaire de Chine] ; Xiao-Ming Jin [République populaire de Chine] ; Xiaofeng Ge [République populaire de Chine]

Source :

Thoracic cancer [ 1759-7714 ] ; 2020.

RBID : pubmed:32096592

Abstract

BACKGROUND

Radioresistance of some non-small cell lung cancer (NSCLC) types increases the risk of recurrence or metastasis in afflicted patients, following radiotherapy. As such, further improvements to NSCLC radiotherapy are needed. The expression of oncogene TP53-regulated inhibitor of apoptosis 1 (TRIAP1) in NSCLC is increased following irradiation. Furthermore, gene set enrichment analysis (GSEA) has suggested that TRIAP1 might be involved in maintaining redox homeostasis. This in turn might enhance cell radioresistance.

METHODS

In this study we irradiated human NSCLC cell lines (A549 and H460), while knocking down TRIAP1, to determine whether a disrupted redox homeostasis could attenuate radioresistance.

RESULTS

Irradiation notably increased both mRNA and protein levels of TRIAP1. In addition, TRIAP1 knockdown decreased the expression of several antioxidant proteins, including thioredoxin-related transmembrane protein (TMX) 1, TMX2, thioredoxin (TXN), glutaredoxin (GLRX) 2, GLRX3, peroxiredoxin (PRDX) 3, PRDX4, and PRDX6 in A549 and H460 cells. In addition, silencing TRIAP1 impaired the radiation-induced increase of the aforementioned proteins. Continuing along this line, we observed a radiation-induced reduction of cell viability and invasion, as well as increased apoptosis and intracellular reactive oxygen species following TRIAP1 knockdown.

CONCLUSIONS

In summary, we identified TRIAP1 as a key contributor to the radioresistance of NSCLC by maintaining redox homeostasis.

DOI: 10.1111/1759-7714.13358
PubMed: 32096592
PubMed Central: PMC7113066

Affiliations:

République populaire de Chine

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Le document en format XML

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<series><title level="j">Thoracic cancer</title>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>Radioresistance of some non-small cell lung cancer (NSCLC) types increases the risk of recurrence or metastasis in afflicted patients, following radiotherapy. As such, further improvements to NSCLC radiotherapy are needed. The expression of oncogene TP53-regulated inhibitor of apoptosis 1 (TRIAP1) in NSCLC is increased following irradiation. Furthermore, gene set enrichment analysis (GSEA) has suggested that TRIAP1 might be involved in maintaining redox homeostasis. This in turn might enhance cell radioresistance.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>In this study we irradiated human NSCLC cell lines (A549 and H460), while knocking down TRIAP1, to determine whether a disrupted redox homeostasis could attenuate radioresistance.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>Irradiation notably increased both mRNA and protein levels of TRIAP1. In addition, TRIAP1 knockdown decreased the expression of several antioxidant proteins, including thioredoxin-related transmembrane protein (TMX) 1, TMX2, thioredoxin (TXN), glutaredoxin (GLRX) 2, GLRX3, peroxiredoxin (PRDX) 3, PRDX4, and PRDX6 in A549 and H460 cells. In addition, silencing TRIAP1 impaired the radiation-induced increase of the aforementioned proteins. Continuing along this line, we observed a radiation-induced reduction of cell viability and invasion, as well as increased apoptosis and intracellular reactive oxygen species following TRIAP1 knockdown.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>In summary, we identified TRIAP1 as a key contributor to the radioresistance of NSCLC by maintaining redox homeostasis.</p>
</div>
</front>
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<pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32096592</PMID>
<DateRevised><Year>2020</Year>
<Month>07</Month>
<Day>15</Day>
</DateRevised>
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<Issue>4</Issue>
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<Title>Thoracic cancer</Title>
<ISOAbbreviation>Thorac Cancer</ISOAbbreviation>
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<ArticleTitle>TRIAP1 knockdown sensitizes non-small cell lung cancer to ionizing radiation by disrupting redox homeostasis.</ArticleTitle>
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<Abstract><AbstractText Label="BACKGROUND">Radioresistance of some non-small cell lung cancer (NSCLC) types increases the risk of recurrence or metastasis in afflicted patients, following radiotherapy. As such, further improvements to NSCLC radiotherapy are needed. The expression of oncogene TP53-regulated inhibitor of apoptosis 1 (TRIAP1) in NSCLC is increased following irradiation. Furthermore, gene set enrichment analysis (GSEA) has suggested that TRIAP1 might be involved in maintaining redox homeostasis. This in turn might enhance cell radioresistance.</AbstractText>
<AbstractText Label="METHODS">In this study we irradiated human NSCLC cell lines (A549 and H460), while knocking down TRIAP1, to determine whether a disrupted redox homeostasis could attenuate radioresistance.</AbstractText>
<AbstractText Label="RESULTS">Irradiation notably increased both mRNA and protein levels of TRIAP1. In addition, TRIAP1 knockdown decreased the expression of several antioxidant proteins, including thioredoxin-related transmembrane protein (TMX) 1, TMX2, thioredoxin (TXN), glutaredoxin (GLRX) 2, GLRX3, peroxiredoxin (PRDX) 3, PRDX4, and PRDX6 in A549 and H460 cells. In addition, silencing TRIAP1 impaired the radiation-induced increase of the aforementioned proteins. Continuing along this line, we observed a radiation-induced reduction of cell viability and invasion, as well as increased apoptosis and intracellular reactive oxygen species following TRIAP1 knockdown.</AbstractText>
<AbstractText Label="CONCLUSIONS">In summary, we identified TRIAP1 as a key contributor to the radioresistance of NSCLC by maintaining redox homeostasis.</AbstractText>
<CopyrightInformation>© 2020 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hao</LastName>
<ForeName>Chun-Cheng</ForeName>
<Initials>CC</Initials>
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<Author ValidYN="Y"><LastName>Luo</LastName>
<ForeName>Jia-Ning</ForeName>
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<AffiliationInfo><Affiliation>Department of Radiotherapy, Harbin Medical University Cancer Hospital, Harbin City, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Cui-Yang</ForeName>
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<AffiliationInfo><Affiliation>Department of Radiotherapy, Harbin Medical University Cancer Hospital, Harbin City, China.</Affiliation>
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<Author ValidYN="Y"><LastName>Zhao</LastName>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Zhong</LastName>
<ForeName>Zhen-Bin</ForeName>
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<Author ValidYN="Y"><LastName>Hu</LastName>
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<Author ValidYN="Y"><LastName>Ge</LastName>
<ForeName>Xiaofeng</ForeName>
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<AffiliationInfo><Affiliation>Department of Radiotherapy, Harbin Medical University Cancer Hospital, Harbin City, China.</Affiliation>
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<Agency>Foundation of Heilongjiang National Health and Family Planning Commission</Agency>
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<affiliations><list><country><li>République populaire de Chine</li>
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<name sortKey="Ge, Xiaofeng" sort="Ge, Xiaofeng" uniqKey="Ge X" first="Xiaofeng" last="Ge">Xiaofeng Ge</name>
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<name sortKey="Jin, Xiao Ming" sort="Jin, Xiao Ming" uniqKey="Jin X" first="Xiao-Ming" last="Jin">Xiao-Ming Jin</name>
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<name sortKey="Zhao, Xin Yu" sort="Zhao, Xin Yu" uniqKey="Zhao X" first="Xin-Yu" last="Zhao">Xin-Yu Zhao</name>
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TRIAP1 knockdown sensitizes non-small cell lung cancer to ionizing radiation by disrupting redox homeostasis.

TRIAP1 knockdown sensitizes non-small cell lung cancer to ionizing radiation by disrupting redox homeostasis.

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