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首页> 外文期刊>Oncology letters >Never in mitosis gene A-related kinase 6 promotes cell proliferation of hepatocellular carcinoma via cyclin B modulation
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Never in mitosis gene A-related kinase 6 promotes cell proliferation of hepatocellular carcinoma via cyclin B modulation

机译:有丝分裂基因A相关激酶6从不通过细胞周期蛋白B调节促进肝细胞癌的细胞增殖

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摘要

Never in mitosis gene A-related kinase (Nek) 6 is a recently identified Nek that is required for mitotic cell cycle progression; however, the role and mechanism of Nek6 activity during hepatocarcinogenesis is not well known. The aim of this study was to investigate the potential roles and internal mechanism of Nek6 in hepatocellular carcinoma (HCC) development. In the present study, Nek6 was found to be overexpressed in HCC samples and cell lines by florescent real-time quantitative polymerase chain reaction, immunohistochemistry and western blot analysis. Furthermore, it was evidenced to contribute to oncogenesis and progression. The ectopic overexpression of Nek6 promoted cell proliferation and colony formation, whereas gene silencing of Nek6 inhibited these phenotypes, as documented in Huh7, PLC/PRF/5, Hep3B and HepG2 HCC cell lines. Mechanistic analyses indicated that Nek6 regulates the transcription of cyclin B through cdc2 activation, and promotes the accumulation of G0/G1-phase cells. In conclusion, the findings of the current study suggested that Nek6 contributes to the oncogenic potential of HCC, and may present as a potential therapeutic target in this disease.
机译:最近鉴定出的有丝分裂细胞周期进展所需要的Nek从未出现在有丝分裂基因A相关激酶(Nek)6中。但是,尚不清楚Nek6活性在肝癌发生过程中的作用和机制。本研究的目的是研究Nek6在肝细胞癌(HCC)发育中的潜在作用及其内部机制。在本研究中,通过荧光实时定量聚合酶链反应,免疫组织化学和蛋白质印迹分析,发现Nek6在HCC样品和细胞系中过表达。此外,已证明其有助于肿瘤发生和进展。如Huh7,PLC / PRF / 5,Hep3B和HepG2 HCC细胞株所示,Nek6的异位过表达促进细胞增殖和集落形成,而Nek6的基因沉默则抑制了这些表型。机理分析表明,Nek6通过cdc2激活调节细胞周期蛋白B的转录,并促进G0 / G1期细胞的蓄积。总之,本研究的结果表明,Nek6有助于肝癌的致癌潜力,并且可能作为该疾病的潜在治疗靶标。

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