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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">HIPK1 drives p53 activation to limit colorectal cancer cell growth</title><author><name sortKey="Rey, Christophe" sort="Rey, Christophe" uniqKey="Rey C" first="Christophe" last="Rey">Christophe Rey</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation></author><author><name sortKey="Soubeyran, Isabelle" sort="Soubeyran, Isabelle" uniqKey="Soubeyran I" first="Isabelle" last="Soubeyran">Isabelle Soubeyran</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Département de Biopathologie; Institut Bergonié; Bordeaux, France</nlm:aff></affiliation></author><author><name sortKey="Mahouche, Isabelle" sort="Mahouche, Isabelle" uniqKey="Mahouche I" first="Isabelle" last="Mahouche">Isabelle Mahouche</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation></author><author><name sortKey="Pedeboscq, Stephane" sort="Pedeboscq, Stephane" uniqKey="Pedeboscq S" first="Stephane" last="Pedeboscq">Stephane Pedeboscq</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Hopital Saint-André; CHU Bordeaux; Bordeaux, France</nlm:aff></affiliation></author><author><name sortKey="Bessede, Alban" sort="Bessede, Alban" uniqKey="Bessede A" first="Alban" last="Bessede">Alban Bessede</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation></author><author><name sortKey="Ichas, Francois" sort="Ichas, Francois" uniqKey="Ichas F" first="François" last="Ichas">François Ichas</name><affiliation><nlm:aff id="A4">FluoFarma; Pessac, France</nlm:aff></affiliation></author><author><name sortKey="De Giorgi, Francesca" sort="De Giorgi, Francesca" uniqKey="De Giorgi F" first="Francesca" last="De Giorgi">Francesca De Giorgi</name><affiliation><nlm:aff id="A4">FluoFarma; Pessac, France</nlm:aff></affiliation></author><author><name sortKey="Lartigue, Lydia" sort="Lartigue, Lydia" uniqKey="Lartigue L" first="Lydia" last="Lartigue">Lydia Lartigue</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23676219</idno><idno type="pmc">3735702</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735702</idno><idno type="RBID">PMC:3735702</idno><idno type="doi">10.4161/cc.24927</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">000443</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000443</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">HIPK1 drives p53 activation to limit colorectal cancer cell growth</title><author><name sortKey="Rey, Christophe" sort="Rey, Christophe" uniqKey="Rey C" first="Christophe" last="Rey">Christophe Rey</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation></author><author><name sortKey="Soubeyran, Isabelle" sort="Soubeyran, Isabelle" uniqKey="Soubeyran I" first="Isabelle" last="Soubeyran">Isabelle Soubeyran</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Département de Biopathologie; Institut Bergonié; Bordeaux, France</nlm:aff></affiliation></author><author><name sortKey="Mahouche, Isabelle" sort="Mahouche, Isabelle" uniqKey="Mahouche I" first="Isabelle" last="Mahouche">Isabelle Mahouche</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation></author><author><name sortKey="Pedeboscq, Stephane" sort="Pedeboscq, Stephane" uniqKey="Pedeboscq S" first="Stephane" last="Pedeboscq">Stephane Pedeboscq</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Hopital Saint-André; CHU Bordeaux; Bordeaux, France</nlm:aff></affiliation></author><author><name sortKey="Bessede, Alban" sort="Bessede, Alban" uniqKey="Bessede A" first="Alban" last="Bessede">Alban Bessede</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</nlm:aff></affiliation></author><author><name sortKey="Ichas, Francois" sort="Ichas, Francois" uniqKey="Ichas F" first="François" last="Ichas">François Ichas</name><affiliation><nlm:aff id="A4">FluoFarma; Pessac, France</nlm:aff></affiliation></author><author><name sortKey="De Giorgi, Francesca" sort="De Giorgi, Francesca" uniqKey="De Giorgi F" first="Francesca" last="De Giorgi">Francesca De Giorgi</name><affiliation><nlm:aff id="A4">FluoFarma; Pessac, France</nlm:aff></affiliation></author><author><name sortKey="Lartigue, Lydia" sort="Lartigue, Lydia" uniqKey="Lartigue L" first="Lydia" last="Lartigue">Lydia Lartigue</name><affiliation><nlm:aff id="A1">INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</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="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>HIPK1 (homeodomain interacting protein kinase 1) is a serine/threonine kinase that belongs to the CMGC superfamily. Emerging data point to the role of HIPK1 in cancer, but it is still not clear whether it acts as a tumor suppressor or promoter. Here we identified HIPK1 as a kinase that is significantly overexpressed in colorectal cancer (CRC) and whose expression is stage-dependent. Being abundantly expressed at the onset of the disease, the HIPK1 level gradually decreased as tumor stage progressed. To further uncover how this factor regulates tumorigenesis and establish whether it constitutes an early factor necessary for neoplastic transformation or for cellular defense, we studied the effect of its overexpression in vitro by investigating various cancer-related signaling cascades. We found that HIPK1 mostly regulates the p53 signaling pathway both in HCT116 and HeLa cells. By phosphorylating p53 on its serine-15, HIPK1 favored its transactivation potential, which led to a rise in p21 protein level and a decline in cell proliferation. Assuming that HIPK1 could impede CRC growth by turning on the p53/p21 pathway, we then checked p21 mRNA levels in patients. Interestingly, p21 transcripts were only increased in a subset of patients expressing high levels of HIPK1. Unlike the rest of the cohort, the majority of these patients hosted a native p53 protein, meaning that such a pro-survival pathway (HIPK1+ > p53 > p21) is active in patients, and that HIPK1 acts rather as a tumor suppressor.</p></div></front></TEI><pmc article-type="research-article"><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">CC</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>Landes Bioscience</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23676219</article-id><article-id pub-id-type="pmc">3735702</article-id><article-id pub-id-type="publisher-id">2012CC4722R</article-id><article-id pub-id-type="doi">10.4161/cc.24927</article-id><article-id pub-id-type="pii">24927</article-id><article-categories><subj-group subj-group-type="heading"><subject>Report</subject></subj-group></article-categories><title-group><article-title>HIPK1 drives p53 activation to limit colorectal cancer cell growth</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Rey</surname><given-names>Christophe</given-names></name><xref ref-type="aff" rid="A1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Soubeyran</surname><given-names>Isabelle</given-names></name><xref ref-type="aff" rid="A1"><sup>1</sup></xref><xref ref-type="aff" rid="A2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Mahouche</surname><given-names>Isabelle</given-names></name><xref ref-type="aff" rid="A1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Pedeboscq</surname><given-names>Stephane</given-names></name><xref ref-type="aff" rid="A1"><sup>1</sup></xref><xref ref-type="aff" rid="A3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Bessede</surname><given-names>Alban</given-names></name><xref ref-type="aff" rid="A1"><sup>1</sup></xref><xref ref-type="author-notes" rid="afn0"><sup>†</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ichas</surname><given-names>François</given-names></name><xref ref-type="aff" rid="A4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>De Giorgi</surname><given-names>Francesca</given-names></name><xref ref-type="aff" rid="A4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Lartigue</surname><given-names>Lydia</given-names></name><xref ref-type="aff" rid="A1"><sup>1</sup></xref><xref ref-type="corresp" rid="cor1">*</xref></contrib><aff id="A1"><label>1</label>INSERM U916; Institut Bergonié; Université de Bordeaux; Bordeaux, France</aff><aff id="A2"><label>2</label>Département de Biopathologie; Institut Bergonié; Bordeaux, France</aff><aff id="A3"><label>3</label>Hopital Saint-André; CHU Bordeaux; Bordeaux, France</aff><aff id="A4"><label>4</label>FluoFarma; Pessac, France</aff></contrib-group><author-notes><fn id="afn0"><label>†</label><p>Current affiliation: Neuroinflammation Group; Department of Pharmacology; University New South Wales; Sydney, NSW Australia</p></fn><corresp id="cor1"><label>*</label>Correspondence to: Lydia Lartigue, Email: <email xlink:href="l.lartigue-faustin@bordeaux.unicancer.fr">l.lartigue-faustin@bordeaux.unicancer.fr</email></corresp></author-notes><pub-date pub-type="ppub"><day>15</day><month>6</month><year>2013</year></pub-date><pub-date pub-type="epub"><day>15</day><month>5</month><year>2013</year></pub-date><volume>12</volume><issue>12</issue><fpage>1879</fpage><lpage>1891</lpage><history><date date-type="received"><day>28</day><month>12</month><year>2012</year></date><date date-type="rev-recd"><day>03</day><month>5</month><year>2013</year></date><date date-type="accepted"><day>03</day><month>5</month><year>2013</year></date></history><permissions><copyright-statement>Copyright © 2013 Landes Bioscience</copyright-statement><copyright-year>2013</copyright-year></permissions><abstract><p>HIPK1 (homeodomain interacting protein kinase 1) is a serine/threonine kinase that belongs to the CMGC superfamily. Emerging data point to the role of HIPK1 in cancer, but it is still not clear whether it acts as a tumor suppressor or promoter. Here we identified HIPK1 as a kinase that is significantly overexpressed in colorectal cancer (CRC) and whose expression is stage-dependent. Being abundantly expressed at the onset of the disease, the HIPK1 level gradually decreased as tumor stage progressed. To further uncover how this factor regulates tumorigenesis and establish whether it constitutes an early factor necessary for neoplastic transformation or for cellular defense, we studied the effect of its overexpression in vitro by investigating various cancer-related signaling cascades. We found that HIPK1 mostly regulates the p53 signaling pathway both in HCT116 and HeLa cells. By phosphorylating p53 on its serine-15, HIPK1 favored its transactivation potential, which led to a rise in p21 protein level and a decline in cell proliferation. Assuming that HIPK1 could impede CRC growth by turning on the p53/p21 pathway, we then checked p21 mRNA levels in patients. Interestingly, p21 transcripts were only increased in a subset of patients expressing high levels of HIPK1. Unlike the rest of the cohort, the majority of these patients hosted a native p53 protein, meaning that such a pro-survival pathway (HIPK1+ > p53 > p21) is active in patients, and that HIPK1 acts rather as a tumor suppressor.</p></abstract><kwd-group kwd-group-type="author"><title>Keywords: </title><kwd>HIPK1</kwd><kwd>p53</kwd><kwd>p21</kwd><kwd>growth arrest</kwd><kwd>colorectal cancer</kwd><kwd>tumor suppressor</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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