Centre of Imaging Diagnosis, Guangxi Medical University Cancer Hospital, Nanning, Guangxi 530021, China.
Departments of Ultrasound, Guangxi Medical University Cancer Hospital, Nanning, Guangxi 530021, China.
Biomed Res Int. 2020 Sep 5;2020:3280530. doi: 10.1155/2020/3280530. eCollection 2020.
Hepatocellular carcinoma (HCC) is one of the most highly aggressive cancer worldwide with an extremely poor prognosis. Evidence has revealed that () is abnormally expressed in a series of cancers. However, its expressions and functions in HCC have not been clearly acknowledged.
We detected the expression level of both in the Gene Expression Omnibus (GEO) database and 86 paired clinical HCC tissues together with paired adjacent normal tissues by quantitative real-time PCR (qRT-PCR). Afterwards, the transfected HCC cell line SMMC-7721 cells were collected for the cell proliferation assay, cell-cycle arrest, cell migration, and invasion assays to explore the roles of in regulating cellular function. In addition, bioinformatics analysis, combined with qRT-PCR and dual-luciferase reporter assays, were performed to confirm whether ribosomal protein SA () mRNA was the direct target gene of . Moreover, the Cancer Genome Atlas (TCGA) and GEO databases as well as 86 paired clinical HCC tissues were used to verify the negative regulation between and .
In the present study, both the GEO database (GSE36915 and GSE74618) analysis and qRT-PCR analysis of 86 paired clinical tissues showed that was significantly downregulated in HCC tissues. The overexpression of inhibited proliferation, cell cycle, migration, and invasion in SMMC-7721 cells. In addition, miR-587 directly interacted with the 3'-untranslated region (UTR) of . Moreover, overexpression directly suppressed expression, and the two genes were inversely expressed in HCC based on the analyses in TCGA and GEO (GSE36376) databases and qPCR analysis of 86 paired clinical tissues.
Our results demonstrate that is downexpressed in HCC and regulates the cellular function by targeting .
肝细胞癌(HCC)是全球侵袭性最强、预后极差的癌症之一。有证据表明,()在一系列癌症中异常表达。然而,其在 HCC 中的表达和功能尚未明确。
我们通过定量实时 PCR(qRT-PCR)检测了基因表达综合数据库(GEO)和 86 对配对的 HCC 组织及配对的相邻正常组织中两者的表达水平。随后,对转染的 HCC 细胞系 SMMC-7721 细胞进行细胞增殖、细胞周期阻滞、细胞迁移和侵袭实验,以探讨在调节细胞功能中()的作用。此外,通过生物信息学分析,结合 qRT-PCR 和双荧光素酶报告基因实验,证实核糖体蛋白 SA()mRNA 是否为的直接靶基因。此外,还使用癌症基因组图谱(TCGA)和 GEO 数据库以及 86 对配对的 HCC 组织来验证和之间的负调控关系。
在本研究中,GEO 数据库(GSE36915 和 GSE74618)分析和 86 对配对临床组织的 qRT-PCR 分析均表明,在 HCC 组织中显著下调。在 SMMC-7721 细胞中过表达可抑制增殖、细胞周期、迁移和侵袭。此外,miR-587 可直接与的 3'-非翻译区(UTR)相互作用。此外,过表达可直接抑制的表达,并且这两个基因在 TCGA 和 GEO(GSE36376)数据库的分析以及对 86 对配对临床组织的 qPCR 分析中呈反向表达。
我们的研究结果表明,在 HCC 中下调,并通过靶向调控细胞功能。