German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany; Heidelberg University, 69120 Heidelberg, Germany.
Heidelberg University, 69120 Heidelberg, Germany; Molecular Neurobiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Cell Rep. 2020 Apr 14;31(2):107504. doi: 10.1016/j.celrep.2020.03.068.
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.
细胞生长与有丝分裂增殖的哺乳动物细胞的细胞周期进程相偶联,但其中的分子机制尚不清楚。CyclinD-Cdk4/6 已知可磷酸化 RB 以促进 S 期进入,但最近的研究表明它们具有其他功能。我们在这里表明,CyclinD-Cdk4/6 通过结合并磷酸化 TSC2 的 Ser1217 和 Ser1452 来激活 mTORC1。Cdk4/6 的药理学抑制导致多种人类和小鼠细胞系(包括乳腺癌细胞)中 mTORC1 活性的快速、TSC2 依赖性降低。通过同时驱动 mTORC1 和 E2F,CyclinD-Cdk4/6 将细胞生长与细胞周期进程偶联。与此一致,我们发现增殖的成年啮齿动物大脑中的神经干细胞中 mTORC1 活性是细胞周期依赖性的。我们发现 Cdk4/6 抑制通过 TSC2 和 mTORC1 部分减少细胞增殖。这具有临床相关性,因为 Cdk4/6 抑制剂用于乳腺癌治疗。