Livin Regulates H2A.XY142 Phosphorylation and Promotes Autophagy in Colon Cancer Cells via a Novel Kinase Activity
Identifieur interne : 000C76 ( Ncbi/Merge ); précédent : 000C75; suivant : 000C77Livin Regulates H2A.XY142 Phosphorylation and Promotes Autophagy in Colon Cancer Cells via a Novel Kinase Activity
Auteurs : Yang Ge ; Bao-Lin Liu ; Jun-Peng Cui ; Shu-Qiang LiSource :
- Frontiers in Oncology [ 2234-943X ] ; 2019.
Abstract
Url:
DOI: 10.3389/fonc.2019.01233
PubMed: 31799193
PubMed Central: 6868062
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Livin Regulates H2A.X<sup>Y142</sup>
Phosphorylation and Promotes Autophagy in Colon Cancer Cells via a Novel Kinase Activity</title>
<author><name sortKey="Ge, Yang" sort="Ge, Yang" uniqKey="Ge Y" first="Yang" last="Ge">Yang Ge</name>
</author>
<author><name sortKey="Liu, Bao Lin" sort="Liu, Bao Lin" uniqKey="Liu B" first="Bao-Lin" last="Liu">Bao-Lin Liu</name>
</author>
<author><name sortKey="Cui, Jun Peng" sort="Cui, Jun Peng" uniqKey="Cui J" first="Jun-Peng" last="Cui">Jun-Peng Cui</name>
</author>
<author><name sortKey="Li, Shu Qiang" sort="Li, Shu Qiang" uniqKey="Li S" first="Shu-Qiang" last="Li">Shu-Qiang Li</name>
</author>
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<idno type="doi">10.3389/fonc.2019.01233</idno>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Livin Regulates H2A.X<sup>Y142</sup>
Phosphorylation and Promotes Autophagy in Colon Cancer Cells via a Novel Kinase Activity</title>
<author><name sortKey="Ge, Yang" sort="Ge, Yang" uniqKey="Ge Y" first="Yang" last="Ge">Yang Ge</name>
</author>
<author><name sortKey="Liu, Bao Lin" sort="Liu, Bao Lin" uniqKey="Liu B" first="Bao-Lin" last="Liu">Bao-Lin Liu</name>
</author>
<author><name sortKey="Cui, Jun Peng" sort="Cui, Jun Peng" uniqKey="Cui J" first="Jun-Peng" last="Cui">Jun-Peng Cui</name>
</author>
<author><name sortKey="Li, Shu Qiang" sort="Li, Shu Qiang" uniqKey="Li S" first="Shu-Qiang" last="Li">Shu-Qiang Li</name>
</author>
</analytic>
<series><title level="j">Frontiers in Oncology</title>
<idno type="eISSN">2234-943X</idno>
<imprint><date when="2019">2019</date>
</imprint>
</series>
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<front><div type="abstract" xml:lang="en"><p><bold>Objective:</bold>
To investigate Livin-mediated regulation of H2A.X<sup>Y142</sup>
phosphorylation via a novel kinase activity and its effect on autophagy in colon cancer cells.</p>
<p><bold>Methods:</bold>
The interaction between Livin and H2A.X was tested by immunoprecipitation. H2A.X–/– HCT116 cells were transfected with human influenza hemagglutinin (HA)-tagged WT or Y142F phospho-dead mutantH2A.X plasmids. GST-tagged recombinant Livin protein was used to perform <italic>in vitro</italic>
pull-down experiment and kinase assay. H2A.X–/–Livin+/+ SW480 cells were co-transfected with H2A.X<sup>WT</sup>
/H2A.X<sup>Y142F</sup>
plasmid and LC3 EGFP-tagged plasmid to explore whether H2A.X<sup>Y142F</sup>
was involved in Livin-mediated autophagy induced by starvation in colon cancer cells.</p>
<p><bold>Results:</bold>
Co-immunoprecipitation studies confirmed that Livin interacted with H2A.X and that it was phosphorylation dependent. <italic>In vitro</italic>
kinase assay confirmed that Livin could phosphorylate H2A.X. Knockdown of Livin (Livin–/–) in SW480 cells or HCT116 cells canceled the starvation-induced autophagy in colon cancer cells; H2A.X–/–Livin+/+ SW480 cells transfected with H2A.X<sup>WT</sup>
activated autophagy induced by starvation while cells transfected with H2A.X<sup>Y142F</sup>
had no significant difference; Livin-H2A.X<sup>Y142F</sup>
axis activated autophagy in colon cancer cells through transcriptionally regulating <italic>ATG5</italic>
and <italic>ATG7</italic>
.</p>
<p><bold>Conclusion:</bold>
Livin promotes autophagy in colon cancer cells via regulating the phosphorylation of H2A.X<sup>Y142</sup>
.</p>
</div>
</front>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Oncol</journal-id>
<journal-id journal-id-type="iso-abbrev">Front Oncol</journal-id>
<journal-id journal-id-type="publisher-id">Front. Oncol.</journal-id>
<journal-title-group><journal-title>Frontiers in Oncology</journal-title>
</journal-title-group>
<issn pub-type="epub">2234-943X</issn>
<publisher><publisher-name>Frontiers Media S.A.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31799193</article-id>
<article-id pub-id-type="pmc">6868062</article-id>
<article-id pub-id-type="doi">10.3389/fonc.2019.01233</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Oncology</subject>
<subj-group><subject>Original Research</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Livin Regulates H2A.X<sup>Y142</sup>
Phosphorylation and Promotes Autophagy in Colon Cancer Cells via a Novel Kinase Activity</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Ge</surname>
<given-names>Yang</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Liu</surname>
<given-names>Bao-lin</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Cui</surname>
<given-names>Jun-peng</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Li</surname>
<given-names>Shu-qiang</given-names>
</name>
<xref ref-type="corresp" rid="c001"><sup>*</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/729644/overview"></uri>
</contrib>
</contrib-group>
<aff><institution>The Six Department of General Surgery, Shengjing Hospital of China Medical University</institution>
,<addr-line>Shenyang</addr-line>
,<country>China</country>
</aff>
<author-notes><fn fn-type="edited-by"><p>Edited by: Massimo Bonora, Albert Einstein College of Medicine, United States</p>
</fn>
<fn fn-type="edited-by"><p>Reviewed by: Guang-Chao Chen, Academia Sinica, Taiwan; Robert Friis, University of Bern, Switzerland</p>
</fn>
<corresp id="c001">*Correspondence: Shu-qiang Li <email>lishuqiang_cmu@163.com</email>
</corresp>
<fn fn-type="other" id="fn001"><p>This article was submitted to Molecular and Cellular Oncology, a section of the journal Frontiers in Oncology</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>14</day>
<month>11</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>9</volume>
<elocation-id>1233</elocation-id>
<history><date date-type="received"><day>09</day>
<month>5</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>28</day>
<month>10</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2019 Ge, Liu, Cui and Li.</copyright-statement>
<copyright-year>2019</copyright-year>
<copyright-holder>Ge, Liu, Cui and Li</copyright-holder>
<license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p>
</license>
</permissions>
<abstract><p><bold>Objective:</bold>
To investigate Livin-mediated regulation of H2A.X<sup>Y142</sup>
phosphorylation via a novel kinase activity and its effect on autophagy in colon cancer cells.</p>
<p><bold>Methods:</bold>
The interaction between Livin and H2A.X was tested by immunoprecipitation. H2A.X–/– HCT116 cells were transfected with human influenza hemagglutinin (HA)-tagged WT or Y142F phospho-dead mutantH2A.X plasmids. GST-tagged recombinant Livin protein was used to perform <italic>in vitro</italic>
pull-down experiment and kinase assay. H2A.X–/–Livin+/+ SW480 cells were co-transfected with H2A.X<sup>WT</sup>
/H2A.X<sup>Y142F</sup>
plasmid and LC3 EGFP-tagged plasmid to explore whether H2A.X<sup>Y142F</sup>
was involved in Livin-mediated autophagy induced by starvation in colon cancer cells.</p>
<p><bold>Results:</bold>
Co-immunoprecipitation studies confirmed that Livin interacted with H2A.X and that it was phosphorylation dependent. <italic>In vitro</italic>
kinase assay confirmed that Livin could phosphorylate H2A.X. Knockdown of Livin (Livin–/–) in SW480 cells or HCT116 cells canceled the starvation-induced autophagy in colon cancer cells; H2A.X–/–Livin+/+ SW480 cells transfected with H2A.X<sup>WT</sup>
activated autophagy induced by starvation while cells transfected with H2A.X<sup>Y142F</sup>
had no significant difference; Livin-H2A.X<sup>Y142F</sup>
axis activated autophagy in colon cancer cells through transcriptionally regulating <italic>ATG5</italic>
and <italic>ATG7</italic>
.</p>
<p><bold>Conclusion:</bold>
Livin promotes autophagy in colon cancer cells via regulating the phosphorylation of H2A.X<sup>Y142</sup>
.</p>
</abstract>
<kwd-group><kwd>Livin</kwd>
<kwd>autophagy</kwd>
<kwd>colon cancer cells</kwd>
<kwd>H2A.X</kwd>
<kwd>phosphorylation</kwd>
</kwd-group>
<counts><fig-count count="5"></fig-count>
<table-count count="0"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="30"></ref-count>
<page-count count="10"></page-count>
<word-count count="5232"></word-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Cui, Jun Peng" sort="Cui, Jun Peng" uniqKey="Cui J" first="Jun-Peng" last="Cui">Jun-Peng Cui</name>
<name sortKey="Ge, Yang" sort="Ge, Yang" uniqKey="Ge Y" first="Yang" last="Ge">Yang Ge</name>
<name sortKey="Li, Shu Qiang" sort="Li, Shu Qiang" uniqKey="Li S" first="Shu-Qiang" last="Li">Shu-Qiang Li</name>
<name sortKey="Liu, Bao Lin" sort="Liu, Bao Lin" uniqKey="Liu B" first="Bao-Lin" last="Liu">Bao-Lin Liu</name>
</noCountry>
</tree>
</affiliations>
</record>
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