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首页> 外文期刊>Journal of Cellular Physiology >Evidence that leptin through STAT and CREB signaling enhances cyclin D1 expression and promotes human endometrial cancer proliferation.
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Evidence that leptin through STAT and CREB signaling enhances cyclin D1 expression and promotes human endometrial cancer proliferation.

机译：瘦素通过统计和分子的证据信号增强细胞周期蛋白D1和表达式促进人类子宫内膜癌扩散。

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摘要

Obesity is a risk factor for endometrial cancer in pre- and post-menopausal women. Leptin, an adipocyte-derived hormone, in addition to the control weight homeostasis, is implicated in multiple biological actions. A recent study demonstrated that leptin promotes endometrial cancer growth and invasiveness through STAT/MAPK and Akt pathways, but the molecular mechanism involved in such processes still needs to be elucidated. In an attempt to understand the role of leptin in regulating endometrial cancer cells proliferation, we have demonstrated that leptin treatment reduced the numbers of cells in G0/G1-phase while increased cell population in S-phase. This effect is associated with an up-regulation of cyclin D1 together with a down-regulation of cyclin-dependent kinase inhibitor p21(WAF1/Cip1). Mutagenesis studies, eletrophoretic mobility shift, and chromatin immunoprecipitation analysis revealed that signal transducers and activators of transcription 3 (STAT3) and cyclic AMP-responsive element (CRE) binding protein motifs, within cyclin D1 promoter, were required for leptin-induced cyclin D1 expression in Ishikawa endometrial cancer cells. Silencing of STAT3 and CREB gene expression by RNA interference reversed the up-regulatory effect of leptin on cyclin D1 expression and cells proliferation. These results support the hypothesis that STAT3 and CREB play an important role in leptin signaling pathway that leads to the proliferation of Ishikawa cells, thus establishing a direct association between obesity and endometrial tumorogenesis.
机译：肥胖是子宫内膜癌的危险因素前和绝经后的妇女。adipocyte-derived激素,除了控制体重体内平衡,有牵连多种生物的行为。表明瘦素促进子宫内膜通过统计/ MAPK癌症生长和侵袭性和Akt通路,但分子机制参与这些过程仍然需要阐明。瘦素在调节子宫内膜癌细胞增殖,表明瘦素治疗细胞数量的减少G0 / g1期而增加的细胞群s阶段。老年病的细胞周期蛋白D1在一起细胞周期蛋白依赖性激酶的下调p21抑制剂(WAF1 / Cip1)。eletrophoretic迁移转变,染色质免疫沉淀反应分析显示信号传感器和转录的活化剂3(STAT3)和循环AMP-responsive元素(CRE)结合蛋白图案,在细胞周期蛋白D1子,leptin-induced所需细胞周期蛋白D1石川子宫内膜癌中表达细胞。表达式通过RNA干扰逆转up-regulatory瘦素对细胞周期蛋白D1的影响表达和细胞增殖。支持假设STAT3和分子瘦素信号通路的一个重要的角色导致石川的扩散细胞,从而建立直接联系肥胖和子宫内膜tumorogenesis之间。

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