HIF-1α and rapamycin act as gerosuppressant in multiple myeloma cells upon genotoxic stress.
Identifieur interne : 001D34 ( PubMed/Checkpoint ); précédent : 001D33; suivant : 001D35HIF-1α and rapamycin act as gerosuppressant in multiple myeloma cells upon genotoxic stress.
Auteurs : Clémence Coudre [France] ; Julien Alani [France] ; William Ritchie [Australie] ; Véronique Marsaud [France] ; Brigitte Sola [France] ; Julie Cahu [France]Source :
- Cell cycle (Georgetown, Tex.) [ 1551-4005 ] ; 2016.
Abstract
Multiple myeloma (MM) is still an incurable hematological malignancy. Despite recent progress due to new anti-myeloma agents, the pathology is characterized by a high frequency of de novo or acquired resistance. Delineating the mechanisms of MM resistance is essential for therapeutic advances. We previously showed that long-term genotoxic stress induces the establishment of a senescence-associated secretory phenotype, a pro-inflammatory response that favors the emergence of cells with cancer stem-like properties. Here, we studied the short-term response of MM cells following treatment with various DNA damaging agents such as the energetic C-ion irradiation. MM cells are highly resistant to all treatments and do not enter apoptosis after they arrest cycling at the G2 phase. Although the DNA damage response pathway was activated, DNA breaks remained chronically in damaged MM cells. We found, using a transcriptomic approach that RAD50, a major DNA repair gene was downregulated early after genotoxic stress. In two gerosuppression situations: induction of hypoxia and inhibition of the mammalian target of rapamycin (mTOR) pathway, we observed, after the treatment with a DNA damaging agent, a normalization of RAD50 expression concomitant with the absence of cell cycle arrest. We propose that combining inhibitors of mTOR with genotoxic agents could avoid MM cells to senesce and secrete pro-inflammatory factors responsible for cancer stem-like cell emergence and, in turn, relapse of MM patients.
DOI: 10.1080/15384101.2016.1196302
PubMed: 27340936
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first="Clémence" last="Coudre">Clémence Coudre</name><affiliation wicri:level="1"><nlm:affiliation>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen </wicri:regionArea><wicri:noRegion>Caen </wicri:noRegion><wicri:noRegion>Caen </wicri:noRegion></affiliation></author><author><name sortKey="Alani, Julien" sort="Alani, Julien" uniqKey="Alani J" first="Julien" last="Alani">Julien Alani</name><affiliation wicri:level="1"><nlm:affiliation>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen </wicri:regionArea><wicri:noRegion>Caen </wicri:noRegion><wicri:noRegion>Caen </wicri:noRegion></affiliation></author><author><name sortKey="Ritchie, William" sort="Ritchie, William" uniqKey="Ritchie W" first="William" last="Ritchie">William Ritchie</name><affiliation wicri:level="1"><nlm:affiliation>b Centenary Institute, University of Sydney , Sydney , Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>b Centenary Institute, University of Sydney , Sydney </wicri:regionArea><wicri:noRegion>Sydney </wicri:noRegion></affiliation></author><author><name sortKey="Marsaud, Veronique" sort="Marsaud, Veronique" uniqKey="Marsaud V" first="Véronique" last="Marsaud">Véronique Marsaud</name><affiliation wicri:level="1"><nlm:affiliation>c Institut Curie, INSERM U1021, CNRS UMR3347 , Orsay , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>c Institut Curie, INSERM U1021, CNRS UMR3347 , Orsay </wicri:regionArea><wicri:noRegion>Orsay </wicri:noRegion><wicri:noRegion>Orsay </wicri:noRegion></affiliation></author><author><name sortKey="Sola, Brigitte" sort="Sola, Brigitte" uniqKey="Sola B" first="Brigitte" last="Sola">Brigitte Sola</name><affiliation wicri:level="1"><nlm:affiliation>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen </wicri:regionArea><wicri:noRegion>Caen </wicri:noRegion><wicri:noRegion>Caen </wicri:noRegion></affiliation></author><author><name sortKey="Cahu, Julie" sort="Cahu, Julie" uniqKey="Cahu J" first="Julie" last="Cahu">Julie Cahu</name><affiliation wicri:level="1"><nlm:affiliation>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen , France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen </wicri:regionArea><wicri:noRegion>Caen </wicri:noRegion><wicri:noRegion>Caen </wicri:noRegion></affiliation></author></analytic><series><title level="j">Cell cycle (Georgetown, Tex.)</title><idno type="eISSN">1551-4005</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Multiple myeloma (MM) is still an incurable hematological malignancy. Despite recent progress due to new anti-myeloma agents, the pathology is characterized by a high frequency of de novo or acquired resistance. Delineating the mechanisms of MM resistance is essential for therapeutic advances. We previously showed that long-term genotoxic stress induces the establishment of a senescence-associated secretory phenotype, a pro-inflammatory response that favors the emergence of cells with cancer stem-like properties. Here, we studied the short-term response of MM cells following treatment with various DNA damaging agents such as the energetic C-ion irradiation. MM cells are highly resistant to all treatments and do not enter apoptosis after they arrest cycling at the G2 phase. Although the DNA damage response pathway was activated, DNA breaks remained chronically in damaged MM cells. We found, using a transcriptomic approach that RAD50, a major DNA repair gene was downregulated early after genotoxic stress. In two gerosuppression situations: induction of hypoxia and inhibition of the mammalian target of rapamycin (mTOR) pathway, we observed, after the treatment with a DNA damaging agent, a normalization of RAD50 expression concomitant with the absence of cell cycle arrest. We propose that combining inhibitors of mTOR with genotoxic agents could avoid MM cells to senesce and secrete pro-inflammatory factors responsible for cancer stem-like cell emergence and, in turn, relapse of MM patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27340936</PMID><DateCreated><Year>2016</Year><Month>07</Month><Day>15</Day></DateCreated><DateRevised><Year>2017</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1551-4005</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>16</Issue><PubDate><Year>2016</Year><Month>Aug</Month><Day>17</Day></PubDate></JournalIssue><Title>Cell cycle (Georgetown, Tex.)</Title><ISOAbbreviation>Cell Cycle</ISOAbbreviation></Journal><ArticleTitle>HIF-1α and rapamycin act as gerosuppressant in multiple myeloma cells upon genotoxic stress.</ArticleTitle><Pagination><MedlinePgn>2174-2182</MedlinePgn></Pagination><Abstract><AbstractText>Multiple myeloma (MM) is still an incurable hematological malignancy. Despite recent progress due to new anti-myeloma agents, the pathology is characterized by a high frequency of de novo or acquired resistance. Delineating the mechanisms of MM resistance is essential for therapeutic advances. We previously showed that long-term genotoxic stress induces the establishment of a senescence-associated secretory phenotype, a pro-inflammatory response that favors the emergence of cells with cancer stem-like properties. Here, we studied the short-term response of MM cells following treatment with various DNA damaging agents such as the energetic C-ion irradiation. MM cells are highly resistant to all treatments and do not enter apoptosis after they arrest cycling at the G2 phase. Although the DNA damage response pathway was activated, DNA breaks remained chronically in damaged MM cells. We found, using a transcriptomic approach that RAD50, a major DNA repair gene was downregulated early after genotoxic stress. In two gerosuppression situations: induction of hypoxia and inhibition of the mammalian target of rapamycin (mTOR) pathway, we observed, after the treatment with a DNA damaging agent, a normalization of RAD50 expression concomitant with the absence of cell cycle arrest. We propose that combining inhibitors of mTOR with genotoxic agents could avoid MM cells to senesce and secrete pro-inflammatory factors responsible for cancer stem-like cell emergence and, in turn, relapse of MM patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Coudre</LastName><ForeName>Clémence</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alani</LastName><ForeName>Julien</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ritchie</LastName><ForeName>William</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>b Centenary Institute, University of Sydney , Sydney , Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marsaud</LastName><ForeName>Véronique</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>c Institut Curie, INSERM U1021, CNRS UMR3347 , Orsay , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sola</LastName><ForeName>Brigitte</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cahu</LastName><ForeName>Julie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>a Normandie Univ, UNICAEN, EA4652, MICAH team , Caen , France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>06</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cell Cycle</MedlineTA><NlmUniqueID>101137841</NlmUniqueID><ISSNLinking>1551-4005</ISSNLinking></MedlineJournalInfo><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Genetics. 1999 May;152(1):143-52</RefSource><PMID Version="1">10224249</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Death Dis. 2012 Dec 20;3:e446</RefSource><PMID Version="1">23254289</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2011 Jun 08;474(7350):230-4</RefSource><PMID Version="1">21654808</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Rep. 2015 Feb 3;10(4):471-83</RefSource><PMID Version="1">25640177</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2015 Mar 19;10(3):e0121581</RefSource><PMID Version="1">25790254</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Leukemia. 2012 Jun;26(6):1436-9</RefSource><PMID 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Dec 22;118(26):6860-70</RefSource><PMID Version="1">22045983</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Blood. 2004 Apr 15;103(8):3138-47</RefSource><PMID Version="1">15070696</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Leukemia. 2012 Dec;26(12):2530-7</RefSource><PMID Version="1">22733078</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Leukemia. 2014 May;28(5):1155-8</RefSource><PMID Version="1">24365790</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>BMB Rep. 2008 Nov 30;41(11):751-6</RefSource><PMID Version="1">19017485</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Cancer Ther. 2009 Jan;8(1):83-93</RefSource><PMID Version="1">19139116</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cancer Cell. 2005 Aug;8(2):99-110</RefSource><PMID Version="1">16098463</PMID></CommentsCorrections></CommentsCorrectionsList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">DNA damage response</Keyword><Keyword MajorTopicYN="N">DNA repair</Keyword><Keyword MajorTopicYN="N">cancer stem-like cell</Keyword><Keyword MajorTopicYN="N">cell cycle arrest</Keyword><Keyword MajorTopicYN="N">irradiation</Keyword><Keyword MajorTopicYN="N">mTOR</Keyword><Keyword MajorTopicYN="N">senescence</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>11</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27340936</ArticleId><ArticleId IdType="doi">10.1080/15384101.2016.1196302</ArticleId><ArticleId IdType="pmc">PMC4993538</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Australie</li><li>France</li></country></list><tree><country name="France"><noRegion><name sortKey="Coudre, Clemence" sort="Coudre, Clemence" uniqKey="Coudre C" first="Clémence" last="Coudre">Clémence Coudre</name></noRegion><name sortKey="Alani, Julien" sort="Alani, Julien" uniqKey="Alani J" first="Julien" last="Alani">Julien Alani</name><name sortKey="Cahu, Julie" sort="Cahu, Julie" uniqKey="Cahu J" first="Julie" last="Cahu">Julie Cahu</name><name sortKey="Marsaud, Veronique" sort="Marsaud, Veronique" uniqKey="Marsaud V" first="Véronique" last="Marsaud">Véronique Marsaud</name><name sortKey="Sola, Brigitte" sort="Sola, Brigitte" uniqKey="Sola B" first="Brigitte" last="Sola">Brigitte Sola</name></country><country name="Australie"><noRegion><name sortKey="Ritchie, 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