| Literature DB >> 32294430 |
Jesús Romero-Pozuelo1, Gianluca Figlia1, Oguzhan Kaya2, Ana Martin-Villalba3, Aurelio A Teleman4.
Abstract
Cell growth is coupled to cell-cycle progression in mitotically proliferating mammalian cells, but the underlying molecular mechanisms are not well understood. CyclinD-Cdk4/6 is known to phosphorylate RB to promote S-phase entry, but recent work suggests they have additional functions. We show here that CyclinD-Cdk4/6 activates mTORC1 by binding and phosphorylating TSC2 on Ser1217 and Ser1452. Pharmacological inhibition of Cdk4/6 leads to a rapid, TSC2-dependent reduction of mTORC1 activity in multiple human and mouse cell lines, including breast cancer cells. By simultaneously driving mTORC1 and E2F, CyclinD-Cdk4/6 couples cell growth to cell-cycle progression. Consistent with this, we see that mTORC1 activity is cell cycle dependent in proliferating neural stem cells of the adult rodent brain. We find that Cdk4/6 inhibition reduces cell proliferation partly via TSC2 and mTORC1. This is of clinical relevance, because Cdk4/6 inhibitors are used for breast cancer therapy.Entities:
Keywords: Cdk4; Cdk6; CycD; TSC2; abemaciclib; cell cycle; cell growth; mTORC1; palbociclib; ribociclib
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Year: 2020 PMID: 32294430 DOI: 10.1016/j.celrep.2020.03.068
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423