4.7 Article

MASTL is enriched in cancerous and pluripotent stem cells and influences OCT1/OCT4 levels

Journal

ISCIENCE
Volume 25, Issue 6, Pages -

Publisher

CELL PRESS
DOI: 10.1016/j.isci.2022.104459

Keywords

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Funding

  1. Academy of Finland [297079, 312517, 337530]
  2. Academy of Finland CoE for Translational Cancer Biology
  3. ERC CoG grant [615258]
  4. Sigrid Juselius Foundation
  5. Finnish Cultural Foundation
  6. Cancer Research UK [A17196]
  7. Stand Up to Cancer campaign for Cancer Research UK [A29800]
  8. EMBO
  9. Finnish Cancer Organization
  10. Academy of Finland (AKA) [312517, 297079] Funding Source: Academy of Finland (AKA)

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MASTL plays an important role in stem cells and breast cancer progression, with its effects mediated through pathways such as TGFBR2 to regulate stemness factors.
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 beta 3 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-beta receptor II (TGFBR2), a key modulator of TGF-beta 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.

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