Inhibition of Glutaredoxin 5 predisposes Cisplatin-resistant Head and Neck Cancer Cells to Ferroptosis.
Identifieur interne : 000103 ( Main/Exploration ); précédent : 000102; suivant : 000104Inhibition of Glutaredoxin 5 predisposes Cisplatin-resistant Head and Neck Cancer Cells to Ferroptosis.
Auteurs : Jaewang Lee [Corée du Sud] ; Ji Hyeon You [Corée du Sud] ; Daiha Shin [Corée du Sud] ; Jong-Lyel Roh [Corée du Sud]Source :
- Theranostics [ 1838-7640 ] ; 2020.
Abstract
Rationale: Loss of iron-sulfur cluster function predisposes cancer cells to ferroptosis by upregulating iron-starvation response, but the role of glutaredoxin 5 (GLRX5) silencing in ferroptosis remains unknown. We examined the role of GLRX5 functional loss in promoting ferroptosis in cisplatin-resistant head and neck cancer (HNC) cells. Methods: The effects of sulfasalazine treatment and GLRX5 gene silencing were tested on HNC cell lines and mouse tumor xenograft models. These effects were analyzed concerning cell viability and death, lipid reactive oxygen species (ROS) and mitochondrial iron production, labile iron pool, mRNA/protein expression, and malondialdehyde assays. Results: Cyst(e)ine deprivation, erastin, or sulfasalazine induced ferroptosis in HNC cells, which was relatively less sensitive in cisplatin-resistant HNC cells. Sulfasalazine or cyst(e)ine deprivation-induced ferroptosis resulted from increased lipid peroxidation and intracellular free iron, which were significantly promoted by short-interfering RNA or short hairpin RNA (shRNA) targeting GLRX5 (P<0.05). GLRX5 silencing activated iron-starvation response and boosted up intracellular free iron through the iron-responsive element-binding activity of increased iron regulatory protein (increased transferrin receptor and decreased ferritin). These effects were rescued by resistant GLRX5 cDNA but not by catalytically inactive mutant GLRX5 K101Q. The same results were noted in an in vivo mouse model transplanted with vector or shGLRX5-transduced HNC cells and treated with sulfasalazine. Conclusion: Our data suggest that inhibition of GLRX5 predisposes therapy-resistant HNC cells to ferroptosis.
DOI: 10.7150/thno.46903
PubMed: 32685019
PubMed Central: PMC7359084
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Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Otorhinolaryngology-Head and Neck Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam</wicri:regionArea><wicri:noRegion>Seongnam</wicri:noRegion></affiliation></author><author><name sortKey="Shin, Daiha" sort="Shin, Daiha" uniqKey="Shin D" first="Daiha" last="Shin">Daiha Shin</name><affiliation wicri:level="3"><nlm:affiliation>Western Seoul Center, Korea Basic Science Institute, Seoul, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Western Seoul Center, Korea Basic Science Institute, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Roh, Jong Lyel" sort="Roh, Jong Lyel" uniqKey="Roh J" first="Jong-Lyel" last="Roh">Jong-Lyel Roh</name><affiliation wicri:level="1"><nlm:affiliation>Department of Otorhinolaryngology-Head and Neck Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Otorhinolaryngology-Head and Neck Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam</wicri:regionArea><wicri:noRegion>Seongnam</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32685019</idno><idno type="pmid">32685019</idno><idno type="doi">10.7150/thno.46903</idno><idno type="pmc">PMC7359084</idno><idno type="wicri:Area/Main/Corpus">000060</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000060</idno><idno 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Ji Hyeon" sort="You, Ji Hyeon" uniqKey="You J" first="Ji Hyeon" last="You">Ji Hyeon You</name><affiliation wicri:level="1"><nlm:affiliation>Department of Otorhinolaryngology-Head and Neck Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Otorhinolaryngology-Head and Neck Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam</wicri:regionArea><wicri:noRegion>Seongnam</wicri:noRegion></affiliation></author><author><name sortKey="Shin, Daiha" sort="Shin, Daiha" uniqKey="Shin D" first="Daiha" last="Shin">Daiha Shin</name><affiliation wicri:level="3"><nlm:affiliation>Western Seoul Center, Korea Basic Science Institute, Seoul, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Western Seoul Center, Korea Basic Science Institute, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Roh, Jong Lyel" sort="Roh, Jong Lyel" uniqKey="Roh J" first="Jong-Lyel" last="Roh">Jong-Lyel Roh</name><affiliation wicri:level="1"><nlm:affiliation>Department of Otorhinolaryngology-Head and Neck Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Otorhinolaryngology-Head and Neck Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam</wicri:regionArea><wicri:noRegion>Seongnam</wicri:noRegion></affiliation></author></analytic><series><title level="j">Theranostics</title><idno type="eISSN">1838-7640</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><b>Rationale:</b> Loss of iron-sulfur cluster function predisposes cancer cells to ferroptosis by upregulating iron-starvation response, but the role of glutaredoxin 5 (GLRX5) silencing in ferroptosis remains unknown. We examined the role of GLRX5 functional loss in promoting ferroptosis in cisplatin-resistant head and neck cancer (HNC) cells. <b>Methods:</b> The effects of sulfasalazine treatment and GLRX5 gene silencing were tested on HNC cell lines and mouse tumor xenograft models. These effects were analyzed concerning cell viability and death, lipid reactive oxygen species (ROS) and mitochondrial iron production, labile iron pool, mRNA/protein expression, and malondialdehyde assays. <b>Results:</b> Cyst(e)ine deprivation, erastin, or sulfasalazine induced ferroptosis in HNC cells, which was relatively less sensitive in cisplatin-resistant HNC cells. Sulfasalazine or cyst(e)ine deprivation-induced ferroptosis resulted from increased lipid peroxidation and intracellular free iron, which were significantly promoted by short-interfering RNA or short hairpin RNA (shRNA) targeting GLRX5 (<i>P</i><0.05). GLRX5 silencing activated iron-starvation response and boosted up intracellular free iron through the iron-responsive element-binding activity of increased iron regulatory protein (increased transferrin receptor and decreased ferritin). These effects were rescued by resistant GLRX5 cDNA but not by catalytically inactive mutant GLRX5 K101Q. The same results were noted in an <i>in vivo</i> mouse model transplanted with vector or shGLRX5-transduced HNC cells and treated with sulfasalazine. <b>Conclusion:</b> Our data suggest that inhibition of GLRX5 predisposes therapy-resistant HNC cells to ferroptosis.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32685019</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1838-7640</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>17</Issue><PubDate><Year>2020</Year></PubDate></JournalIssue><Title>Theranostics</Title><ISOAbbreviation>Theranostics</ISOAbbreviation></Journal><ArticleTitle>Inhibition of Glutaredoxin 5 predisposes Cisplatin-resistant Head and Neck Cancer Cells to Ferroptosis.</ArticleTitle><Pagination><MedlinePgn>7775-7786</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.7150/thno.46903</ELocationID><Abstract><AbstractText><b>Rationale:</b> Loss of iron-sulfur cluster function predisposes cancer cells to ferroptosis by upregulating iron-starvation response, but the role of glutaredoxin 5 (GLRX5) silencing in ferroptosis remains unknown. We examined the role of GLRX5 functional loss in promoting ferroptosis in cisplatin-resistant head and neck cancer (HNC) cells. <b>Methods:</b> The effects of sulfasalazine treatment and GLRX5 gene silencing were tested on HNC cell lines and mouse tumor xenograft models. These effects were analyzed concerning cell viability and death, lipid reactive oxygen species (ROS) and mitochondrial iron production, labile iron pool, mRNA/protein expression, and malondialdehyde assays. <b>Results:</b> Cyst(e)ine deprivation, erastin, or sulfasalazine induced ferroptosis in HNC cells, which was relatively less sensitive in cisplatin-resistant HNC cells. Sulfasalazine or cyst(e)ine deprivation-induced ferroptosis resulted from increased lipid peroxidation and intracellular free iron, which were significantly promoted by short-interfering RNA or short hairpin RNA (shRNA) targeting GLRX5 (<i>P</i><0.05). GLRX5 silencing activated iron-starvation response and boosted up intracellular free iron through the iron-responsive element-binding activity of increased iron regulatory protein (increased transferrin receptor and decreased ferritin). These effects were rescued by resistant GLRX5 cDNA but not by catalytically inactive mutant GLRX5 K101Q. The same results were noted in an <i>in vivo</i> mouse model transplanted with vector or shGLRX5-transduced HNC cells and treated with sulfasalazine. <b>Conclusion:</b> Our data suggest that inhibition of GLRX5 predisposes therapy-resistant HNC cells to ferroptosis.</AbstractText><CopyrightInformation>© The author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Jaewang</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology-Head and Neck Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>You</LastName><ForeName>Ji Hyeon</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology-Head and Neck Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shin</LastName><ForeName>Daiha</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Western Seoul Center, Korea Basic Science Institute, Seoul, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roh</LastName><ForeName>Jong-Lyel</ForeName><Initials>JL</Initials><AffiliationInfo><Affiliation>Department of Otorhinolaryngology-Head and Neck Surgery, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Republic of Korea.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>06</Month><Day>19</Day></ArticleDate></Article><MedlineJournalInfo><Country>Australia</Country><MedlineTA>Theranostics</MedlineTA><NlmUniqueID>101552395</NlmUniqueID><ISSNLinking>1838-7640</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Ferroptosis</Keyword><Keyword MajorTopicYN="Y">cancer cells</Keyword><Keyword MajorTopicYN="Y">free iron</Keyword><Keyword MajorTopicYN="Y">gene silencing</Keyword><Keyword MajorTopicYN="Y">glutaredoxin 5</Keyword></KeywordList><CoiStatement>Competing Interests: The authors have declared that no competing interest exists.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>04</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>05</Month><Day>31</Day></PubMedPubDate><PubMedPubDate 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