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Article: CAMK2A supported tumor initiating cells of lung adenocarcinoma by upregulating SOX2 through EZH2 phosphorylation

TitleCAMK2A supported tumor initiating cells of lung adenocarcinoma by upregulating SOX2 through EZH2 phosphorylation
Authors
KeywordsA-549 cell line
cancer stem cell
cancer survival
cell renewal
controlled study
Issue Date2020
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, 2020, v. 11, p. article no. 410 How to Cite?
AbstractTumor initiating cells (TIC) of lung cancer are mainly induced by stress-related plasticity. Calcium/Calmodulin dependent protein kinase II alpha (CAMK2A) is a key calcium signaling molecule activated by exogenous and endogenous stimuli with effects on multiple cell functions but little is known about its role on TIC. In human lung adenocarcinomas (AD), CAMK2A was aberrantly activated in a proportion of cases and was an independent risk factor predicting shorter survivals. Functionally, CAMK2A enhanced TIC phenotypes in vitro and in vivo. CAMK2A regulated SOX2 expression by reducing H3K27me3 and EZH2 occupancy at SOX2 regulatory regions, leading to its epigenetic de-repression with functional consequences. Further, CAMK2A caused kinase-dependent phosphorylation of EZH2 at T487 with suppression of EZH2 activity. Together, the data demonstrated the CAMK2A-EZH2-SOX2 axis on TIC regulation. This study provided phenotypic and mechanistic evidence for the TIC supportive role of CAMK2A, implicating a novel predictive and therapeutic target for lung cancer.
Persistent Identifierhttp://hdl.handle.net/10722/293872
ISSN
2023 Impact Factor: 8.1
2023 SCImago Journal Rankings: 2.447
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, SQ-
dc.contributor.authorLiu, J-
dc.contributor.authorQin, J-
dc.contributor.authorZHU, Y-
dc.contributor.authorTin, VPC-
dc.contributor.authorYam, JWP-
dc.contributor.authorWong, MP-
dc.contributor.authorXiao, Z-
dc.date.accessioned2020-11-23T08:23:01Z-
dc.date.available2020-11-23T08:23:01Z-
dc.date.issued2020-
dc.identifier.citationCell Death & Disease, 2020, v. 11, p. article no. 410-
dc.identifier.issn2041-4889-
dc.identifier.urihttp://hdl.handle.net/10722/293872-
dc.description.abstractTumor initiating cells (TIC) of lung cancer are mainly induced by stress-related plasticity. Calcium/Calmodulin dependent protein kinase II alpha (CAMK2A) is a key calcium signaling molecule activated by exogenous and endogenous stimuli with effects on multiple cell functions but little is known about its role on TIC. In human lung adenocarcinomas (AD), CAMK2A was aberrantly activated in a proportion of cases and was an independent risk factor predicting shorter survivals. Functionally, CAMK2A enhanced TIC phenotypes in vitro and in vivo. CAMK2A regulated SOX2 expression by reducing H3K27me3 and EZH2 occupancy at SOX2 regulatory regions, leading to its epigenetic de-repression with functional consequences. Further, CAMK2A caused kinase-dependent phosphorylation of EZH2 at T487 with suppression of EZH2 activity. Together, the data demonstrated the CAMK2A-EZH2-SOX2 axis on TIC regulation. This study provided phenotypic and mechanistic evidence for the TIC supportive role of CAMK2A, implicating a novel predictive and therapeutic target for lung cancer.-
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.subjectA-549 cell line-
dc.subjectcancer stem cell-
dc.subjectcancer survival-
dc.subjectcell renewal-
dc.subjectcontrolled study-
dc.titleCAMK2A supported tumor initiating cells of lung adenocarcinoma by upregulating SOX2 through EZH2 phosphorylation-
dc.typeArticle-
dc.identifier.emailWang, SQ: wangsq47@hku.hk-
dc.identifier.emailLiu, J: jingliue@hku.hk-
dc.identifier.emailTin, VPC: pctin@hku.hk-
dc.identifier.emailYam, JWP: judyyam@pathology.hku.hk-
dc.identifier.emailWong, MP: mwpik@hku.hk-
dc.identifier.emailXiao, Z: xiaozj@hku.hk-
dc.identifier.authorityYam, JWP=rp00468-
dc.identifier.authorityWong, MP=rp00348-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41419-020-2553-6-
dc.identifier.pmid32483123-
dc.identifier.pmcidPMC7264342-
dc.identifier.scopuseid_2-s2.0-85085854827-
dc.identifier.hkuros319888-
dc.identifier.hkuros318201-
dc.identifier.volume11-
dc.identifier.spagearticle no. 410-
dc.identifier.epagearticle no. 410-
dc.identifier.isiWOS:000539286100002-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl2041-4889-

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