敲除 NCOA5 可通过抑制上皮间质转化来抑制肝癌细胞的增殖和迁移。
Knockout of NCOA5 impairs proliferation and migration of hepatocellular carcinoma cells by suppressing epithelial-to-mesenchymal transition.
机构信息
Cancer Center, Southern Medical University, Guangzhou, Guangdong, 510315, China; Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, 510315, China.
Cancer Center, Southern Medical University, Guangzhou, Guangdong, 510315, China; Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, 510315, China.
出版信息
Biochem Biophys Res Commun. 2018 Jun 2;500(2):177-183. doi: 10.1016/j.bbrc.2018.04.017. Epub 2018 Apr 14.
Nuclear receptor coactivator 5 (NCOA5) plays important roles in the development of a variety of malignancies. However, the underlying mechanisms remain obscure. In this study, we successfully generated the NCOA5 knockout hepatocellular carcinoma (HCC) cells by CRISPR/Cas9 - mediated genome editing and found that knockout of NCOA5 inhibited the proliferation and tumor microsphere formation of HCC cells significantly. Moreover, the migration ability of NCOA5 knockout HCC cells declined. Mechanistic analyses indicated that knockout of NCOA5 can suppress the epithelial - mesenchymal transition (EMT) in HCC cells. In conclusion, our findings provide a mechanistic insight into the role of NCOA5 in HCC progression.
核受体辅激活因子 5（NCOA5）在多种恶性肿瘤的发生发展中发挥着重要作用。然而，其具体的作用机制尚不清楚。在本研究中，我们成功地利用 CRISPR/Cas9 介导的基因组编辑技术构建了 NCOA5 基因敲除的肝癌细胞系，并发现敲除 NCOA5 可显著抑制肝癌细胞的增殖和肿瘤微球体形成，同时降低肝癌细胞的迁移能力。机制研究表明，敲除 NCOA5 可以抑制肝癌细胞的上皮间质转化（EMT）过程。综上所述，本研究结果为 NCOA5 在肝癌发生发展中的作用机制提供了新的见解。
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