Nuclear cyclin D1: an oncogenic driver in human cancer.
Nuclear cyclin D1: an oncogenic driver in human cancer.
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DOI：
10.1002/jcp.21791
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发表时间：
2009-08
影响因子：
5.6
通讯作者：
Diehl, J. Alan
中科院分区：
文献类型：
--
作者：
Kim, Jong Kyong;Diehl, J. Alan
在人类癌症中经常观察到核心细胞周期机制调节的扰动。细胞周期蛋白D1作为促有丝分裂传感器和CDK 4/6的变构激活剂，是癌症中更频繁改变的细胞周期调节因子之一。细胞周期蛋白D1经常在癌症中过表达，其过表达可归因于许多因素，包括转录，翻译和蛋白质稳定性增加。尽管细胞周期蛋白D1的过度表达与受影响的癌症明显相关，但细胞周期蛋白D1的过度表达不足以驱动致癌转化。相反，新出现的证据表明，细胞周期蛋白D1的细胞核滞留导致改变核运输和蛋白水解是其致癌性的表现至关重要。这篇综述简要概述了目前的数据记录在人类癌症和肿瘤转化的影响异常细胞周期蛋白D1调控的各种机制。
Perturbations in the regulation of the core cell cycle machinery are frequently observed in human cancers. Cyclin D1 which functions as a mitogenic sensor and allosteric activator of CDK4/6, is one of the more frequently altered cell cycle regulators in cancers. Cyclin D1 is frequently overexpressed in cancers and its overexpression can be attributed to many factors including increased transcription, translation, and protein stability. Although cyclin D1 overexpression is clearly implicated in the affected cancers, overexpression of cyclin D1 is not sufficient to drive oncogenic transformation. Rather, emerging evidence suggests that nuclear retention of cyclin D1 resulting from altered nuclear trafficking and proteolysis is critical for the manifestation of its oncogenicity. This review provides a brief overview of current data documenting various mechanisms underlying aberrant cyclin D1 regulation in human cancers and their impact on neoplastic transformation.
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影响因子：
10.5
作者：
Diehl, JA;Zindy, F;Sherr, CJ
通讯作者：
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影响因子：
50.3
作者：
Barbash, Olena;Zamfirova, Petia;Lin, Douglas I.;Chen, Xiangmei;Yang, Ke;Nakagawa, Hiroshi;Lu, Fengmin;Rustgi, Anil K.;Diehl, J. Alan
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Diehl, J. Alan
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影响因子：
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作者：
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通讯作者：
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