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FAK inhibition induces glioblastoma cell senescence-like state through p62 and p27

Permanent lenke
https://hdl.handle.net/10037/24727
DOI
https://doi.org/10.3390/cancers12051086
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article.pdf (3.476Mb)
Publisert versjon (PDF)
Dato
2020-04-27
Type
Journal article
Tidsskriftartikkel
Peer reviewed

Forfatter
Alza, Lía; Nager, Mireia; Visa, Anna; Cantí, Carles; Herreros, Judit
Sammendrag
Focal 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.
Forlag
MDPI
Sitering
Alza, Nager M, Visa, Cantí, Herreros. FAK inhibition induces glioblastoma cell senescence-like state through p62 and p27. Cancers. 2020;12(5)
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  • Artikler, rapporter og annet (medisinsk biologi) [1103]
Copyright 2020 The Author(s)

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