MASTL is enriched in cancerous and pluripotent stem cells and influences OCT1/OCT4 levels.
Cancer
Cell biology
Proteomics
Stem cells research
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
17 Jun 2022
17 Jun 2022
Historique:
received:
04
10
2021
revised:
04
03
2022
accepted:
13
05
2022
entrez:
9
6
2022
pubmed:
10
6
2022
medline:
10
6
2022
Statut:
epublish
Résumé
MASTL is a mitotic accelerator with an emerging role in breast cancer progression. However, the mechanisms behind its oncogenicity remain largely unknown. Here, we identify a previously unknown role and eminent expression of MASTL in stem cells. MASTL staining from a large breast cancer patient cohort indicated a significant association with β3 integrin, an established mediator of breast cancer stemness. MASTL silencing reduced OCT4 levels in human pluripotent stem cells and OCT1 in breast cancer cells. Analysis of the cell-surface proteome indicated a strong link between MASTL and the regulation of TGF-β receptor II (TGFBR2), a key modulator of TGF-β signaling. Overexpression of wild-type and kinase-dead MASTL in normal mammary epithelial cells elevated TGFBR2 levels. Conversely, MASTL depletion in breast cancer cells attenuated TGFBR2 levels and downstream signaling through SMAD3 and AKT pathways. Taken together, these results indicate that MASTL supports stemness regulators in pluripotent and cancerous stem cells.
Identifiants
pubmed: 35677646
doi: 10.1016/j.isci.2022.104459
pii: S2589-0042(22)00730-1
pmc: PMC9167974
doi:
Types de publication
Journal Article
Langues
eng
Pagination
104459Informations de copyright
© 2022 The Author(s).
Déclaration de conflit d'intérêts
The authors declare no competing financial interests.
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