Long noncoding RNA MAPKAPK5-AS1 promotes metastasis through regulation miR-376b-5p/ECT2 axis in hepatocellular carcinoma

被引:3
|
作者
Lv, Enjun
Sheng, Jiaqi
Yu, Chengpeng
Rao, Dean
Huang, Wenjie [1 ]
机构
[1] Huazhong Univ Sci & Technol, Hubei Key Lab Hepatopancreatobiliary Dis, Clin Med Res Ctr Hepat Surg Hubei Prov, Key Lab Organ Transplantat,Minist Educ,Hepat Surg, Wuhan 430030, Hubei, Peoples R China
关键词
HCC; MAPKAPK5-AS1; miR-376b-5p; ECT2; INVASION; LNCRNA;
D O I
10.1016/j.dld.2022.11.024
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background and aims: Hepatocellular carcinoma (HCC) is one of the most common diseases threatening human health worldwide. However, the molecular mechanisms of HCC are still unclear. Here, we identified a differentially expressed lncRNA called MAPKAPK5-AS1(abbreviation: MK5-AS1) and elucidated its role and molecular mechanism in the development of HCC.Methods: Real-time PCR (RT-PCR) was used to verify the expression of MK5-AS1 in hepatocarcinoma cell lines and tumor tissues of HCC patients. The biological functions of MK5-AS1 in HCC cells was assessed both in vitro and in vivo assays. The Lncbase, miRDB and TargetScan databases were used to predict the lncRNA-miRNA-mRNA interactions. RNA immunoprecipitation (RIP) and double luciferase reporter gene assays further verified the interactions.Results: MK5-AS1 expression was significantly upregulated in HCC tissues and cell lines. Furthermore, high MK5-AS1 expression was positively associated with tumor progression and poor prognosis. In vitro and in vivo experiments confirmed that overexpressed MK5-AS1 promoted migration and invasion of HCC cells. Bioinformatics analysis based on Lncbase, miRDB and TargetScan databases showed MK5-AS1 competitively bound to miR-376b-5p that prevented epithelial cell transforming sequence 2 (ECT2) from miRNA-mediated degradation, thus facilitated HCC metastasis.Conclusion: Our results established a tumor promotive role of MK5-AS1 in HCC pathogenesis. & COPY; 2022 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:945 / 954
页数:10
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