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dc.contributor.authorAlza, Lía
dc.contributor.authorNager, Mireia
dc.contributor.authorVisa, Anna
dc.contributor.authorCantí, Carles
dc.contributor.authorHerreros, Judit
dc.date.accessioned2022-04-07T09:26:45Z
dc.date.available2022-04-07T09:26:45Z
dc.date.issued2020-04-27
dc.description.abstractFocal adhesion kinase (FAK) is a central component of focal adhesions that regulate cancer cell proliferation and migration. Here, we studied the effects of FAK inhibition in glioblastoma (GBM), a fast growing brain tumor that has a poor prognosis. Treating GBM cells with the FAK inhibitor PF-573228 induced a proliferative arrest and increased cell size. PF-573228 also reduced the growth of GBM neurospheres. These effects were associated with increased p27/CDKN1B levels and β-galactosidase activity, compatible with acquisition of senescence. Interestingly, FAK inhibition repressed the expression of the autophagy cargo receptor p62/SQSTM-1. Moreover, depleting p62 in GBM cells also induced a senescent-like phenotype through transcriptional upregulation of p27. Our results indicate that FAK inhibition arrests GBM cell proliferation, resulting in cell senescence, and pinpoint p62 as being key to this process. These findings highlight the possible therapeutic value of targeting FAK in GBM.en_US
dc.identifier.citationAlza, Nager M, Visa, Cantí, Herreros. FAK inhibition induces glioblastoma cell senescence-like state through p62 and p27. Cancers. 2020;12(5)
dc.identifier.cristinIDFRIDAID 1889905
dc.identifier.doi10.3390/cancers12051086
dc.identifier.issn2072-6694
dc.identifier.urihttps://hdl.handle.net/10037/24727
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.relation.journalCancers
dc.rights.holderCopyright 2020 The Author(s)en_US
dc.titleFAK inhibition induces glioblastoma cell senescence-like state through p62 and p27en_US
dc.type.versionpublishedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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