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    吴锐, 张斌, 纪明, 张城铭, 刘志毅, 曹宽, 王人颢. CTR9在肝癌中的表达及对肝癌细胞增殖和转移的影响[J]. 徐州医科大学学报, 2021, 41(3): 179-183. DOI: 10.3969/j.issn.2096-3882.2021.03.005
    引用本文: 吴锐, 张斌, 纪明, 张城铭, 刘志毅, 曹宽, 王人颢. CTR9在肝癌中的表达及对肝癌细胞增殖和转移的影响[J]. 徐州医科大学学报, 2021, 41(3): 179-183. DOI: 10.3969/j.issn.2096-3882.2021.03.005
    Effects of CTR9 on the proliferation and metastasis of hepatocellular carcinoma cells[J]. Journal of Xuzhou Medical University, 2021, 41(3): 179-183. DOI: 10.3969/j.issn.2096-3882.2021.03.005
    Citation: Effects of CTR9 on the proliferation and metastasis of hepatocellular carcinoma cells[J]. Journal of Xuzhou Medical University, 2021, 41(3): 179-183. DOI: 10.3969/j.issn.2096-3882.2021.03.005

    CTR9在肝癌中的表达及对肝癌细胞增殖和转移的影响

    Effects of CTR9 on the proliferation and metastasis of hepatocellular carcinoma cells

    • 摘要: 目的研究RNA聚合酶Ⅱ相关因子1复合物(PAF1c)的骨架蛋白CTR9对肝癌细胞增殖、迁移、侵袭调控的分子机制。方法采用Western bolt和免疫组化法检测CTR9在肝癌及癌旁组织中的表达。在HepG2和Huh7细胞中沉默CTR9或瞬时转染外源CTR9。采用EdU实验、集落形成、Transwell实验分析CTR9对肝癌细胞增殖、迁移、侵袭的调控作用。结果CTR9在肝癌组织中呈高表达。沉默CTR9可抑制肝癌细胞的增殖、迁移、侵袭,而过表达CTR9促进肝癌细胞的增殖、迁移、侵袭。CTR9可以正调控Akt/p-Akt。结论通过正向调控Akt/p-Akt,CTR9可促进肝癌细胞的增殖、迁移、侵袭。

       

      Abstract: ObjectiveTo explore the molecular mechanism of CTR9, a core component of PAF1c for RNA Polymerase II regulation,in regulating the proliferation, migration and invasion of hepatocellular carcinoma cells (HCCs).MethodsThe expression of CTR9 in hepatocellular carcinoma and adjacent non-tumor tissues was detected by Western bolt and immunohistochemistry. HepG2 and Huh7 cells were used for CTR9 silencing or transient transfection of exogenous CTR9. Then, EdU assay, colony formation assay, and Transwell assay were used to analyze the regulatory effects of CTR9 on the proliferation, migration and invasion of HCCs. ResultsCTR9 was highly expressed in hepatocellular carcinoma tissues. CTR9 silencing inhibited the proliferation, migration and invasion of HCCs, while overexpression of CTR9 promoted the proliferation, migration and invasion of HCCs. CTR9 positively regulated Akt/p-Akt. ConclusionsCTR9 can promote the proliferation, migration and invasion of HCCs through positively regulating Akt/p-Akt.

       

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