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WNK2 Inhibits Autophagic Flux in Human Glioblastoma Cell Line

2020-02-20Journal article Open access
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dc.contributor.authorAlves, Ana Laura Vieira
dc.contributor.authorCosta, Angela Margarida
dc.contributor.authorMartinho, Olga
dc.contributor.authorda Silva, Vinicius Duval
dc.contributor.authorJordan, Peter
dc.contributor.authorSilva, Viviane Aline Oliveira
dc.contributor.authorReis, Rui Manuel
dc.date.accessioned2021-03-06T15:37:51Z
dc.date.available2021-03-06T15:37:51Z
dc.date.issued2020-02-20
dc.description.abstractAutophagy is a cell-survival pathway with dual role in tumorigenesis, promoting either tumor survival or tumor death. WNK2 gene, a member of the WNK (with no lysine (K)) subfamily, acts as a tumor suppressor gene in gliomas, regulating cell migration and invasion; however, its role in autophagy process is poorly explored. The WNK2-methylated human glioblastoma cell line A172 WT (wild type) was compared to transfected clones A172 EV (empty vector), and A172 WNK2 (WNK2 overexpression) for the evaluation of autophagy using an inhibitor (bafilomycin A1-baf A1) and an inducer (everolimus) of autophagic flux. Western blot and immunofluorescence approaches were used to monitor autophagic markers, LC3A/B and SQSTM1/p62. A172 WNK2 cells presented a significant decrease in LC3B and p62 protein levels, and in LC3A/B ratio when compared with control cells, after treatment with baf A1 + everolimus, suggesting that WNK2 overexpression inhibits the autophagic flux in gliomas. The mTOR pathway was also evaluated under the same conditions, and the observed results suggest that the inhibition of autophagy mediated by WNK2 occurs through a mTOR-independent pathway. In conclusion, the evaluation of the autophagic process demonstrated that WNK2 inhibits the autophagic flux in glioblastoma cell line.pt_PT
dc.description.sponsorshipThis project was supported by the Barretos Cancer Hospital Internal Research Funds (PAIP) to Rui Manuel Reis and by the Public Ministry of Labor Campinas (Research, Prevention, and Education of Occupational Cancer Project), Campinas, Brazil. Ana Laura Vieira Alves is the recipient of a FAPESP master fellowship (2016/18907-0).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationCells. 2020 Feb 20;9(2):485. doi: 10.3390/cells9020485.pt_PT
dc.identifier.doi10.3390/cells9020485pt_PT
dc.identifier.issn2073-4409
dc.identifier.urihttp://hdl.handle.net/10400.18/7344
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherMDPIpt_PT
dc.relation.publisherversionhttps://www.mdpi.com/2073-4409/9/2/485pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectWNK2pt_PT
dc.subjectWNK Protein Kinasept_PT
dc.subjectAutophagypt_PT
dc.subjectAutophagic Fluxpt_PT
dc.subjectGlioblastoma Cell Linept_PT
dc.subjectInhibitionpt_PT
dc.subjectGliomapt_PT
dc.subjectVias de Transdução de Sinal e Patologias Associadaspt_PT
dc.titleWNK2 Inhibits Autophagic Flux in Human Glioblastoma Cell Linept_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.issue2pt_PT
oaire.citation.startPage485pt_PT
oaire.citation.titleCellspt_PT
oaire.citation.volume9pt_PT
rcaap.embargofctAcesso de acordo com política editorial da revista.pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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