Cyclin D1 and cyclin D-dependent kinases enhance oral keratinocyte proliferation but do not block keratinocyte differentiation.

Cyclin D1 and cyclin D-dependent kinases enhance oral keratinocyte proliferation but do not block keratinocyte differentiation.
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DOI:
10.3892/ijo_00000799
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发表时间:
2010-12
影响因子:
5.2
通讯作者:
Mallya SM
Mallya SM
中科院分区:
医学2区
文献类型:
--
作者:
Woods M;Pant R;Mallya SM

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口腔上皮稳态的维持需要细胞增殖和分化之间的良好平衡。然而,耦合这些过程的分子机制及其在肿瘤发生中的失调尚不完全清楚。 Cyclin D1 及其激酶伙伴 CDK4 和 CDK6 在调节细胞周期的 G1-S 期中发挥重要作用。细胞周期蛋白 D1 失调是口腔鳞状细胞癌中的常见事件。在这里,我们检查了细胞周期蛋白 D1、CDK4 和 CDK6 的过度表达是否可以解除口腔角质形成细胞增殖和分化之间的联系。我们的结果表明,细胞周期蛋白 D1 及其激酶伙伴 CDK4 和 CDK6 增强角质形成细胞增殖,但不足以阻止钙诱导的角质形成细胞分化,并且表明单独解除这些 G1 调节激酶的调节不足以解开增殖和分化之间的联系。
Maintenance of oral epithelial homeostasis requires a fine balance between cell proliferation and differentiation. However, the molecular mechanisms that couple these processes, and its deregulation in tumorigenesis are not fully understood. Cyclin D1 and its kinase partners CDK4 and CDK6 play an important role in regulating the G1-S phase of the cell cycle. Deregulation of cyclin D1 is a frequent event in oral squamous cell carcinoma. Here, we examined whether overexpression of cyclin D1, CDK4 and CDK6 can deregulate the link between oral keratinocyte proliferation and differentiation. Our results show that cyclin D1 and its kinase partners CDK4 and CDK6 enhance keratinocyte proliferation, but are not sufficient to block calcium-induced keratinocyte differentiation and suggest that deregulation of these G1-regulatory kinases alone is insufficient to uncouple the link between proliferation and differentiation.
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