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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">HIF-1α and rapamycin act as gerosuppressant in multiple myeloma cells upon genotoxic stress</title><author><name sortKey="Coudre, Clemence" sort="Coudre, Clemence" uniqKey="Coudre C" first="Clémence" last="Coudre">Clémence Coudre</name><affiliation><nlm:aff id="af0001"><institution>Normandie Univ, UNICAEN, EA4652, MICAH team</institution>, Caen,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Alani, Julien" sort="Alani, Julien" uniqKey="Alani J" first="Julien" last="Alani">Julien Alani</name><affiliation><nlm:aff id="af0001"><institution>Normandie Univ, UNICAEN, EA4652, MICAH team</institution>, Caen,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Ritchie, William" sort="Ritchie, William" uniqKey="Ritchie W" first="William" last="Ritchie">William Ritchie</name><affiliation><nlm:aff id="af0002"><institution>Centenary Institute, University of Sydney</institution>, Sydney,<country>Australia</country></nlm:aff></affiliation></author><author><name sortKey="Marsaud, Veronique" sort="Marsaud, Veronique" uniqKey="Marsaud V" first="Véronique" last="Marsaud">Véronique Marsaud</name><affiliation><nlm:aff id="af0003"><institution>Institut Curie, INSERM U1021, CNRS UMR3347</institution>, Orsay,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Sola, Brigitte" sort="Sola, Brigitte" uniqKey="Sola B" first="Brigitte" last="Sola">Brigitte Sola</name><affiliation><nlm:aff id="af0001"><institution>Normandie Univ, UNICAEN, EA4652, MICAH team</institution>, Caen,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Cahu, Julie" sort="Cahu, Julie" uniqKey="Cahu J" first="Julie" last="Cahu">Julie Cahu</name><affiliation><nlm:aff id="af0001"><institution>Normandie Univ, UNICAEN, EA4652, MICAH team</institution>, Caen,<country>France</country></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">27340936</idno><idno type="pmc">4993538</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4993538</idno><idno type="RBID">PMC:4993538</idno><idno type="doi">10.1080/15384101.2016.1196302</idno><date when="2016">2016</date><idno type="wicri:Area/Pmc/Corpus">001369</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001369</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">HIF-1α and rapamycin act as gerosuppressant in multiple myeloma cells upon genotoxic stress</title><author><name sortKey="Coudre, Clemence" sort="Coudre, Clemence" uniqKey="Coudre C" first="Clémence" last="Coudre">Clémence Coudre</name><affiliation><nlm:aff id="af0001"><institution>Normandie Univ, UNICAEN, EA4652, MICAH team</institution>, Caen,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Alani, Julien" sort="Alani, Julien" uniqKey="Alani J" first="Julien" last="Alani">Julien Alani</name><affiliation><nlm:aff id="af0001"><institution>Normandie Univ, UNICAEN, EA4652, MICAH team</institution>, Caen,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Ritchie, William" sort="Ritchie, William" uniqKey="Ritchie W" first="William" last="Ritchie">William Ritchie</name><affiliation><nlm:aff id="af0002"><institution>Centenary Institute, University of Sydney</institution>, Sydney,<country>Australia</country></nlm:aff></affiliation></author><author><name sortKey="Marsaud, Veronique" sort="Marsaud, Veronique" uniqKey="Marsaud V" first="Véronique" last="Marsaud">Véronique Marsaud</name><affiliation><nlm:aff id="af0003"><institution>Institut Curie, INSERM U1021, CNRS UMR3347</institution>, Orsay,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Sola, Brigitte" sort="Sola, Brigitte" uniqKey="Sola B" first="Brigitte" last="Sola">Brigitte Sola</name><affiliation><nlm:aff id="af0001"><institution>Normandie Univ, UNICAEN, EA4652, MICAH team</institution>, Caen,<country>France</country></nlm:aff></affiliation></author><author><name sortKey="Cahu, Julie" sort="Cahu, Julie" uniqKey="Cahu J" first="Julie" last="Cahu">Julie Cahu</name><affiliation><nlm:aff id="af0001"><institution>Normandie Univ, UNICAEN, EA4652, MICAH team</institution>, Caen,<country>France</country></nlm:aff></affiliation></author></analytic><series><title level="j">Cell Cycle</title><idno type="ISSN">1538-4101</idno><idno type="eISSN">1551-4005</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>ABSTRACT</title><p>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 <italic>de novo</italic> 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 <italic>RAD50</italic>, 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.</p></div></front></TEI><pmc article-type="report"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Cell Cycle</journal-id><journal-id journal-id-type="iso-abbrev">Cell Cycle</journal-id><journal-id journal-id-type="publisher-id">KCCY</journal-id><journal-id journal-id-type="publisher-id">kccy20</journal-id><journal-title-group><journal-title>Cell Cycle</journal-title></journal-title-group><issn pub-type="ppub">1538-4101</issn><issn pub-type="epub">1551-4005</issn><publisher><publisher-name>Taylor & Francis</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">27340936</article-id><article-id pub-id-type="pmc">4993538</article-id><article-id pub-id-type="publisher-id">1196302</article-id><article-id pub-id-type="doi">10.1080/15384101.2016.1196302</article-id><article-categories><subj-group subj-group-type="heading"><subject>Reports</subject></subj-group></article-categories><title-group><article-title>HIF-1α and rapamycin act as gerosuppressant in multiple myeloma cells upon genotoxic stress</article-title><alt-title alt-title-type="running-authors">C. COUDRE ET AL.</alt-title><alt-title alt-title-type="running-title">CELL CYCLE</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Coudre</surname><given-names>Clémence</given-names></name><xref ref-type="aff" rid="af0001"><sup>a</sup></xref><xref ref-type="author-notes" rid="afn0002"><sup>†</sup></xref></contrib><contrib contrib-type="author"><name><surname>Alani</surname><given-names>Julien</given-names></name><xref ref-type="aff" rid="af0001"><sup>a</sup></xref><xref ref-type="author-notes" rid="afn0002"><sup>†</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ritchie</surname><given-names>William</given-names></name><xref ref-type="aff" rid="af0002"><sup>b</sup></xref><xref ref-type="author-notes" rid="afn0003"><sup>††</sup></xref></contrib><contrib contrib-type="author"><name><surname>Marsaud</surname><given-names>Véronique</given-names></name><xref ref-type="aff" rid="af0003"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Sola</surname><given-names>Brigitte</given-names></name><xref ref-type="aff" rid="af0001"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Cahu</surname><given-names>Julie</given-names></name><xref ref-type="aff" rid="af0001"><sup>a</sup></xref></contrib><aff id="af0001"><label>a</label><institution>Normandie Univ, UNICAEN, EA4652, MICAH team</institution>, Caen,<country>France</country></aff><aff id="af0002"><label>b</label><institution>Centenary Institute, University of Sydney</institution>, Sydney,<country>Australia</country></aff><aff id="af0003"><label>c</label><institution>Institut Curie, INSERM U1021, CNRS UMR3347</institution>, Orsay,<country>France</country></aff></contrib-group><author-notes><corresp id="an0001"><bold>CONTACT</bold> Brigitte Sola <email xlink:href="brigitte.sola@unicaen.fr">brigitte.sola@unicaen.fr</email>; Julie Cahu <email xlink:href="julie.cahu@gmail.com">julie.cahu@gmail.com</email><addr-line>EA4642, MICAH team, UFR de médecine, CHU Côte de Nacre</addr-line>, 14032 CAEN Cedex, <country>France</country>.</corresp><fn id="afn0002"><label>†</label><p>These authors contributed equally to the study</p></fn><fn id="afn0003"><label>††</label><p>Present address: Institut de Génomique Fonctionnelle, Montpellier, France</p></fn><fn id="afn0001"><p>Supplemental data for this article can be accessed on the <ext-link ext-link-type="uri" xlink:href="http://www.tandfonline.com/kccy">publisher's website</ext-link>.</p></fn></author-notes><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>24</day><month>6</month><year>2016</year></pub-date><volume>15</volume><issue>16</issue><fpage seq="16">2174</fpage><lpage>2182</lpage><history><date date-type="received"><day>3</day><month>2</month><year>2016</year></date><date date-type="rev-recd"><day>23</day><month>5</month><year>2016</year></date><date date-type="accepted"><day>25</day><month>5</month><year>2016</year></date></history><permissions><copyright-statement>© 2016 Taylor & Francis</copyright-statement><copyright-year>2016</copyright-year><copyright-holder>Taylor & Francis</copyright-holder></permissions><self-uri content-type="pdf" xlink:href="kccy-15-16-1196302.pdf"></self-uri><abstract><title>ABSTRACT</title><p>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 <italic>de novo</italic> 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 <italic>RAD50</italic>, 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.</p></abstract><kwd-group kwd-group-type="author"><title>KEYWORDS</title><kwd>cancer stem-like cell</kwd><kwd>cell cycle arrest</kwd><kwd>DNA damage response</kwd><kwd>DNA repair</kwd><kwd>irradiation</kwd><kwd>mTOR</kwd><kwd>senescence</kwd></kwd-group><counts><fig-count count="3"></fig-count><table-count count="1"></table-count><ref-count count="51"></ref-count><page-count count="9"></page-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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