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首页> 外文期刊>American Journal of Cancer Research >Inhibitor of binding/differentiation 2 (Id2) is regulated by CCAAT/enhancer-binding protein-?± (C/EBP?±) and promotes the proliferation of hepatocellular carcinoma
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Inhibitor of binding/differentiation 2 (Id2) is regulated by CCAAT/enhancer-binding protein-?± (C/EBP?±) and promotes the proliferation of hepatocellular carcinoma

机译:结合/分化抑制剂2(Id2)受CCAAT /增强子结合蛋白-α±(C /EBPβ±)的调节,并促进肝细胞癌的增殖

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摘要

Inhibitor of DNA binding/differentiation (Id2) is an important regulator involved in the initiation and progression of cancer. However, the function and mechanism of the regulation of Id2 in hepatocellular carcinoma (HCC) was unclear. In the present study, we found that the overexpression of Id2 increased HCC cell proliferation in vitro and in vivo. Knockdown of Id2 inhibited HCC cell proliferation in vitro and in vivo. Furthermore, knockdown of Id2 enhanced sorafenib-induced apoptosis in HCC. Conversely, overexpression of Id2 weakened sorafenib-induced apoptosis in HCC. In addition, the transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα) bound to the Id2 promoter and decreased its expression in HCC cells. Therefore, all results suggest that Id2 promotes the proliferation of HCC cells by inhibiting cell apoptosis. Id2 may serve as a potential target in HCC therapy.
机译:DNA结合/分化抑制剂(Id2)是与癌症的发生和发展有关的重要调节剂。然而,尚不清楚肝细胞癌(HCC)中Id2调控的功能和机制。在本研究中,我们发现Id2的过表达增加了体外和体内HCC细胞的增殖。在体外和体内,抑制Id2抑制HCC细胞增殖。此外,Id2的敲除增强了索拉非尼诱导的HCC细胞凋亡。相反,Id2的过表达减弱了索拉非尼诱导的HCC细胞凋亡。此外,转录因子CCAAT /增强子结合蛋白α(C /EBPα)与Id2启动子结合并降低其在HCC细胞中的表达。因此,所有结果表明,Id2通过抑制细胞凋亡来促进HCC细胞的增殖。 Id2可能成为HCC治疗中的潜在靶标。

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