细胞周期蛋白D1通过调控细胞周期退出触发乳腺癌细胞的自主生长。
Cyclin D1 triggers autonomous growth of breast cancer cells by governing cell cycle exit.
作者信息
Zwijsen R M, Klompmaker R, Wientjens E B, Kristel P M, van der Burg B, Michalides R J
机构信息
Department of Tumor Biology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
出版信息
Mol Cell Biol. 1996 Jun;16(6):2554-60. doi: 10.1128/MCB.16.6.2554.
Abstract
Cyclin D1 controls G1-associated processes, including G0-to-G1 and G1-to-S transitions. This study demonstrates a novel aspect of cyclin D1 as a regulator of the transition between G1 and G0. Overexpression of cyclin D1 in MCF7 breast tumor cells resulted in a continued proliferation under low-serum conditions, whereas nonoverexpressing cells ceased to grow. This difference in growth was due to a reduced exit from G1 to G0 in cyclin D1-overexpressing cells. Our data therefore suggest a model in which cyclin D1 overexpression in tumor cells is responsible for hyperproliferation under growth factor-deprived conditions.
摘要
细胞周期蛋白D1控制与G1期相关的过程，包括从G0期到G1期以及从G1期到S期的转变。本研究揭示了细胞周期蛋白D1作为G1期和G0期之间转变调节因子的一个新方面。在MCF7乳腺肿瘤细胞中过表达细胞周期蛋白D1导致在低血清条件下持续增殖，而未过表达的细胞则停止生长。这种生长差异是由于过表达细胞周期蛋白D1的细胞从G1期进入G0期的比例降低。因此，我们的数据提示了一个模型，其中肿瘤细胞中细胞周期蛋白D1的过表达导致在生长因子缺乏的条件下过度增殖。
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Overexpression of mouse D-type cyclins accelerates G1 phase in rodent fibroblasts.小鼠D型细胞周期蛋白的过表达加速了啮齿动物成纤维细胞的G1期。
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