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长链非编码 RNA SNHG1 通过海绵吸附 miR-195-5p 来调节肝细胞癌中 PDCD4 的表达,作为竞争性内源性 RNA 发挥作用。

Long non-coding RNA SNHG1 functions as a competitive endogenous RNA to regulate PDCD4 expression by sponging miR-195-5p in hepatocellular carcinoma.

机构信息

Department of Hepatobiliary Surgery, Changyi People's Hospital of Shandong Province, China.

Department of Infectious Disease, Changyi People's Hospital of Shandong Province, China.

出版信息

Gene. 2019 Sep 25;714:143994. doi: 10.1016/j.gene.2019.143994. Epub 2019 Jul 19.

Abstract

Long non-coding RNA (lncRNA) potentially regulates tumorigenesis. LncRNA small nucleolar RNA host gene 1 (SNHG1) expression remains high in hepatocellular carcinoma cells; however, its biological mechanism in hepatocellular carcinoma remains unknown. In this study, SNHG1 expression in hepatocellular carcinoma cells was detected by qRT-PCR. Proliferative and migratory potentials of hepatocellular carcinoma cells were determined by CCK-8 and Transwell assay, respectively. Then, the nude mice model of xenograft was employed to verify the effect of SNHG1 on tumor formation in vivo. We identified the potential target of SNHG1 through bioinformatics and dual-luciferase reporter gene. Furthermore, Western blot and RIP assay was used for clarifying their interaction and functions in regulating the development of hepatocellular carcinoma. Our results indicated a high expression of SNHG1 in hepatocellular carcinoma cells. Downregulation of SNHG1 inhibited proliferative and migratory potentials of hepatocellular carcinoma cells in vitro and in vivo. Moreover, the expression of programmed cell death 4 (PDCD4) was positively regulated by SNHG1 through competing with miR-195-5p. These results indicated that SNHG1 participated in the development of hepatocellular carcinoma as a ceRNA to competitively bind to miR-195-5p and thus mediate PDCD4 expression.

摘要

长链非编码 RNA(lncRNA)可能调节肿瘤发生。lncRNA 小核仁 RNA 宿主基因 1(SNHG1)在肝癌细胞中表达仍然较高;然而,其在肝癌中的生物学机制尚不清楚。在本研究中,通过 qRT-PCR 检测肝癌细胞中的 SNHG1 表达。通过 CCK-8 和 Transwell 测定分别检测肝癌细胞的增殖和迁移潜能。然后,使用裸鼠异种移植模型来验证 SNHG1 对体内肿瘤形成的影响。我们通过生物信息学和双荧光素酶报告基因鉴定了 SNHG1 的潜在靶标。此外,Western blot 和 RIP 测定用于阐明它们在调节肝癌发展中的相互作用和功能。我们的结果表明 SNHG1 在肝癌细胞中高表达。下调 SNHG1 抑制肝癌细胞的体外和体内增殖和迁移潜能。此外,程序性细胞死亡 4(PDCD4)的表达通过与 miR-195-5p 竞争而被 SNHG1 正向调节。这些结果表明,SNHG1 作为 ceRNA 参与肝癌的发展,通过与 miR-195-5p 竞争结合来调节 PDCD4 的表达。

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