Enhanced p62-NRF2 Feedback Loop due to Impaired Autophagic Flux Contributes to Arsenic-Induced Malignant Transformation of Human Keratinocytes
Identifieur interne : 000837 ( Main/Exploration ); précédent : 000836; suivant : 000838Enhanced p62-NRF2 Feedback Loop due to Impaired Autophagic Flux Contributes to Arsenic-Induced Malignant Transformation of Human Keratinocytes
Auteurs : Xiafang Wu [République populaire de Chine] ; Ru Sun [République populaire de Chine] ; Huihui Wang [République populaire de Chine] ; Bei Yang [République populaire de Chine] ; Fang Wang [République populaire de Chine] ; Hongtao Xu [République populaire de Chine] ; Shimin Chen [République populaire de Chine] ; Rui Zhao [République populaire de Chine] ; Jingbo Pi [République populaire de Chine] ; Yuanyuan Xu [République populaire de Chine]Source :
- Oxidative Medicine and Cellular Longevity [ 1942-0900 ] ; 2019.
Abstract
Chronic exposure to arsenic induces a variety of cancers, particularly in the skin. Autophagy is a highly conserved process which plays a dual role in tumorigenesis. In the present study, we found that chronic exposure to an environmentally relevant dose of arsenite induced malignant transformation of human keratinocytes (HaCaT) with dysregulated autophagy as indicated by an increased number of autophagosomes, activation of mTORC1 pathway, and elevated protein levels of p62 and LC3II. Meanwhile, arsenite-transformed cells showed lower intracellular levels of reactive oxygen species compared with control. Silencing
Url:
DOI: 10.1155/2019/1038932
PubMed: 31781319
PubMed Central: 6875345
Affiliations:
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xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The First Hospital of China Medical University</wicri:regionArea></affiliation></author><author><name sortKey="Sun, Ru" sort="Sun, Ru" uniqKey="Sun R" first="Ru" last="Sun">Ru Sun</name><affiliation wicri:level="1"><nlm:aff id="I1">School of Public Health, China Medical University, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Public Health, China Medical University</wicri:regionArea><wicri:noRegion>China Medical University</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Huihui" sort="Wang, Huihui" uniqKey="Wang H" first="Huihui" last="Wang">Huihui Wang</name><affiliation wicri:level="1"><nlm:aff id="I1">School of Public Health, China Medical University, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Public Health, China Medical University</wicri:regionArea><wicri:noRegion>China Medical University</wicri:noRegion></affiliation></author><author><name sortKey="Yang, Bei" sort="Yang, Bei" uniqKey="Yang B" first="Bei" last="Yang">Bei Yang</name><affiliation wicri:level="1"><nlm:aff id="I3">College of Basic Medical Sciences, China Medical University, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Basic Medical Sciences, China Medical University</wicri:regionArea><wicri:noRegion>China Medical University</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Fang" sort="Wang, Fang" uniqKey="Wang F" first="Fang" last="Wang">Fang Wang</name><affiliation wicri:level="1"><nlm:aff id="I1">School of Public Health, China Medical University, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Public Health, China Medical University</wicri:regionArea><wicri:noRegion>China Medical University</wicri:noRegion></affiliation></author><author><name sortKey="Xu, Hongtao" sort="Xu, Hongtao" uniqKey="Xu H" first="Hongtao" last="Xu">Hongtao Xu</name><affiliation wicri:level="1"><nlm:aff id="I3">College of Basic Medical Sciences, China Medical University, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Basic Medical Sciences, China Medical University</wicri:regionArea><wicri:noRegion>China Medical University</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Shimin" sort="Chen, Shimin" uniqKey="Chen S" first="Shimin" last="Chen">Shimin Chen</name><affiliation wicri:level="1"><nlm:aff id="I1">School of Public Health, China Medical University, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Public Health, China Medical University</wicri:regionArea><wicri:noRegion>China Medical University</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Rui" sort="Zhao, Rui" uniqKey="Zhao R" first="Rui" last="Zhao">Rui Zhao</name><affiliation wicri:level="1"><nlm:aff id="I4">School of Forensic Medicine, China Medical University, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Forensic Medicine, China Medical University</wicri:regionArea><wicri:noRegion>China Medical University</wicri:noRegion></affiliation></author><author><name sortKey="Pi, Jingbo" sort="Pi, Jingbo" uniqKey="Pi J" first="Jingbo" last="Pi">Jingbo Pi</name><affiliation wicri:level="1"><nlm:aff id="I1">School of Public Health, China Medical University, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Public Health, China Medical University</wicri:regionArea><wicri:noRegion>China Medical University</wicri:noRegion></affiliation></author><author><name sortKey="Xu, Yuanyuan" sort="Xu, Yuanyuan" uniqKey="Xu Y" first="Yuanyuan" last="Xu">Yuanyuan Xu</name><affiliation wicri:level="1"><nlm:aff id="I1">School of Public Health, China Medical University, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Public Health, China Medical University</wicri:regionArea><wicri:noRegion>China Medical University</wicri:noRegion></affiliation></author></analytic><series><title level="j">Oxidative Medicine and Cellular Longevity</title><idno type="ISSN">1942-0900</idno><idno type="eISSN">1942-0994</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Chronic exposure to arsenic induces a variety of cancers, particularly in the skin. Autophagy is a highly conserved process which plays a dual role in tumorigenesis. In the present study, we found that chronic exposure to an environmentally relevant dose of arsenite induced malignant transformation of human keratinocytes (HaCaT) with dysregulated autophagy as indicated by an increased number of autophagosomes, activation of mTORC1 pathway, and elevated protein levels of p62 and LC3II. Meanwhile, arsenite-transformed cells showed lower intracellular levels of reactive oxygen species compared with control. Silencing <italic>p62</italic> ameliorated elevation in mRNA levels of NRF2 downstream genes (<italic>AKR1C1</italic> and <italic>NQO1</italic>) and malignant phenotypes (acquired invasiveness and anchor-independent growth) induced by chronic arsenite exposure. On the other hand, silencing <italic>NRF2</italic> abrogated the increase in mRNA and protein levels of p62 and malignant phenotypes induced by arsenite. In response to acute arsenite exposure, impaired autophagic flux with an increase in p62 protein level and interrupted autophagosome-lysosome fusion was observed. The increase in p62 protein levels in response to arsenite was not completely dependent on NRF2 activation and at least partially attributed to protein degradation. Our data indicate that accumulation of p62 by impaired autophagic flux is involved in the activation of NRF2 and contributes to skin tumorigenesis due to chronic arsenite exposure.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Platanias, L C" uniqKey="Platanias L">L. C. Platanias</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Alain, G" uniqKey="Alain G">G. Alain</name></author><author><name sortKey="Tousignant, J" uniqKey="Tousignant J">J. Tousignant</name></author><author><name sortKey="Rozenfarb, E" uniqKey="Rozenfarb E">E. 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Petitgas</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wu, Xiafang" sort="Wu, Xiafang" uniqKey="Wu X" first="Xiafang" last="Wu">Xiafang Wu</name></noRegion><name sortKey="Chen, Shimin" sort="Chen, Shimin" uniqKey="Chen S" first="Shimin" last="Chen">Shimin Chen</name><name sortKey="Pi, Jingbo" sort="Pi, Jingbo" uniqKey="Pi J" first="Jingbo" last="Pi">Jingbo Pi</name><name sortKey="Sun, Ru" sort="Sun, Ru" uniqKey="Sun R" first="Ru" last="Sun">Ru Sun</name><name sortKey="Wang, Fang" sort="Wang, Fang" uniqKey="Wang F" first="Fang" last="Wang">Fang Wang</name><name sortKey="Wang, Huihui" sort="Wang, Huihui" uniqKey="Wang H" first="Huihui" last="Wang">Huihui Wang</name><name sortKey="Wu, Xiafang" sort="Wu, Xiafang" uniqKey="Wu X" first="Xiafang" last="Wu">Xiafang Wu</name><name sortKey="Xu, Hongtao" sort="Xu, Hongtao" uniqKey="Xu H" first="Hongtao" last="Xu">Hongtao Xu</name><name sortKey="Xu, Yuanyuan" sort="Xu, Yuanyuan" uniqKey="Xu Y" first="Yuanyuan" last="Xu">Yuanyuan Xu</name><name sortKey="Yang, Bei" sort="Yang, Bei" uniqKey="Yang B" first="Bei" last="Yang">Bei Yang</name><name sortKey="Zhao, Rui" sort="Zhao, Rui" uniqKey="Zhao R" first="Rui" last="Zhao">Rui Zhao</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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