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Article: Cellular energy stress induces AMPK-mediated regulation of glioblastoma cell proliferation by PIKE-A phosphorylation

TitleCellular energy stress induces AMPK-mediated regulation of glioblastoma cell proliferation by PIKE-A phosphorylation
Authors
Keywordscell cycle arrest
cell energy
cell proliferation
cell stress
cellular distribution
Issue Date2019
PublisherNature Publishing Group: Open Access Journals - Option C. The Journal's web site is located at http://www.nature.com/cddis/index.html
Citation
Cell Death & Disease, 2019, v. 10 n. 3, p. article no. 222 How to Cite?
AbstractPhosphoinositide 3-kinase enhancer-activating Akt (PIKE-A), which associates with and potentiates Akt activity, is a pro-oncogenic factor that play vital role in cancer cell survival and growth. However, PIKE-A physiological functions under energy/nutrient deficiency are poorly understood. The AMP-activated protein kinase (AMPK) is an evolutionarily conserved serine/threonine kinase that is a principal regulator of energy homeostasis and has a critical role in metabolic disorders and cancers. In this present study, we show that cellular energy stress induces PIKE-A phosphorylation mediated by AMPK activation, thereby preventing its carcinogenic action. Moreover, AMPK directly phosphorylates PIKE-A Ser-351 and Ser-377, which become accessible for the interaction with 14-3-3β, and in turn stimulates nuclear translocation of PIKE-A. Nuclear PIKE-A associates with CDK4 and then disrupts CDK4-cyclinD1 complex and inhibits the Rb pathway, resulting in cancer cell cycle arrest. Our data uncover a molecular mechanism and functional significance of PIKE-A phosphorylation response to cellular energy status mediated by AMPK.
Persistent Identifierhttp://hdl.handle.net/10722/277896
ISSN
2017 Impact Factor: 5.638
2015 SCImago Journal Rankings: 2.484
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorZhang, S-
dc.contributor.authorSheng, H-
dc.contributor.authorZhang, X-
dc.contributor.authorQi, Q-
dc.contributor.authorChan, CB-
dc.contributor.authorLi, L-
dc.contributor.authorShan, C-
dc.contributor.authorYe, K-
dc.date.accessioned2019-10-04T08:03:30Z-
dc.date.available2019-10-04T08:03:30Z-
dc.date.issued2019-
dc.identifier.citationCell Death & Disease, 2019, v. 10 n. 3, p. article no. 222-
dc.identifier.issn2041-4889-
dc.identifier.urihttp://hdl.handle.net/10722/277896-
dc.description.abstractPhosphoinositide 3-kinase enhancer-activating Akt (PIKE-A), which associates with and potentiates Akt activity, is a pro-oncogenic factor that play vital role in cancer cell survival and growth. However, PIKE-A physiological functions under energy/nutrient deficiency are poorly understood. The AMP-activated protein kinase (AMPK) is an evolutionarily conserved serine/threonine kinase that is a principal regulator of energy homeostasis and has a critical role in metabolic disorders and cancers. In this present study, we show that cellular energy stress induces PIKE-A phosphorylation mediated by AMPK activation, thereby preventing its carcinogenic action. Moreover, AMPK directly phosphorylates PIKE-A Ser-351 and Ser-377, which become accessible for the interaction with 14-3-3β, and in turn stimulates nuclear translocation of PIKE-A. Nuclear PIKE-A associates with CDK4 and then disrupts CDK4-cyclinD1 complex and inhibits the Rb pathway, resulting in cancer cell cycle arrest. Our data uncover a molecular mechanism and functional significance of PIKE-A phosphorylation response to cellular energy status mediated by AMPK.-
dc.languageeng-
dc.publisherNature Publishing Group: Open Access Journals - Option C. The Journal's web site is located at http://www.nature.com/cddis/index.html-
dc.relation.ispartofCell Death & Disease-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectcell cycle arrest-
dc.subjectcell energy-
dc.subjectcell proliferation-
dc.subjectcell stress-
dc.subjectcellular distribution-
dc.titleCellular energy stress induces AMPK-mediated regulation of glioblastoma cell proliferation by PIKE-A phosphorylation-
dc.typeArticle-
dc.identifier.emailChan, CB: chancb@hku.hk-
dc.identifier.authorityChan, CB=rp02140-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41419-019-1452-1-
dc.identifier.pmid30833542-
dc.identifier.pmcidPMC6399291-
dc.identifier.scopuseid_2-s2.0-85062382609-
dc.identifier.hkuros306544-
dc.identifier.volume10-
dc.identifier.issue3-
dc.identifier.spagearticle no. 222-
dc.identifier.epagearticle no. 222-
dc.publisher.placeUnited Kingdom-

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