Research Article

TRIM45抑制非小细胞肺癌的发展

卷 20, 期 4, 2020

页: [299 - 306] 页: 8

弟呕挨: 10.2174/1566524019666191017143833

价格: $65

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摘要

背景:以前,我们首先确定了包含人三方基序的蛋白45(TRIM45)在有丝分裂原激活的蛋白激酶(MAPK)信号传导途径中起着新的转录阻遏物的作用。此后,TRIM45在肿瘤发展中的抑制作用逐渐显现。然而,TRIM45在肺癌的肿瘤发生中的功能尚未被表征。 方法和结果:在这项研究中,我们发现TRIM45在早期人类非小细胞肺癌(NSCLC)组织中上调。 TRIM45在肺癌细胞中的过表达诱导G1阻滞并促进细胞凋亡,并伴有RB,p16,p53,p27Kip1和Caspase3的表达上调以及CyclinE1和CyclinE2的表达下调。 MAPK信号通路中分子表达的进一步检测表明,肺癌细胞中TRIM45的过表达促进了磷酸化的p38(p-p38)活化并抑制了磷酸化的ERK(p-ERK)活化。据此,在肺癌组织中p-p38增加而p-ERK减少。 结论:这些发现表明TRIM45在肺癌的肿瘤发生中具有抑制作用。 TRIM45在肺癌组织中的高表达可能通过激活p38信号促进细胞凋亡,并通过下调p-ERK抑制增殖,为理解肺癌的发生提供了新的线索。

关键词: TRIM45,NSCLC,肺癌,细胞凋亡,抑制作用,MAPK途径。

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