LncRNA CDKN2B-AS1 Promotes Cell Viability, Migration, and Invasion of Hepatocellular Carcinoma via Sponging miR-424-5p

被引：19

作者：

Shen, Xinying ^{[1
]}

Li, Yong ^{[1
]}

He, Fan ^{[1
]}

Kong, Jian ^{[1
]}

机构：

[1] Shenzhen Peoples Hosp, Dept Intervent Radiol, Shenzhen 518020, Guangdong, Peoples R China

来源：

CANCER MANAGEMENT AND RESEARCH | 2020年 / 12卷

关键词：

lncRNA CDKN2B-AS1; miR-424-5p; migration; invasion; hepatocellular carcinoma; LONG NONCODING RNA; CANCER; ASSOCIATION; PROGRESSION; METASTASIS; GROWTH; SNAIL;

D O I：

10.2147/CMAR.S240000

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Objective: Hepatocellular carcinoma (HCC) results in high mortality and metastasis. In this study, the effects of long non-coding RNA (lncRNA) CDKN2B-AS1 on the progression of HCC were investigated. Materials and Methods: LncRNA CDKN2B-AS1 expression of HCC cancer and adjacent tissues, and HCC cells were detected. Subsequently, CDKN2B-AS1 was overexpressed and silenced in HCC cells to observe the effects of CDKN2B-AS1 on the cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT) of HCC cells by performing cell counting kit-8 (CCK-8), wound-healing, Transwell, and Western blot. The target gene of CDKN2B-AS1 was predicted and verified to be miR-424-5p, whose expression in HCC cells with up- or down-regulation of CDKN2B-AS1 expression was determined. Moreover, the effects of miR-424-5p on cell viability, migration, and invasion and EMT of HCC cells were investigated with miR-424-5p up-regulation or down-regulation, together with overexpression or silencing of CDKN2B-AS1. Results: CDKN2B-AS1 expression was increased in HCC tissues and cells. Silencing of CDKN2B-AS1 suppressed cell viability, migration, invasion, and EMT, while overexpression of CDKN2B-AS1 produced the opposite results. Furthermore, CDKN2B-AS1 was predicted and verified to target miR-424-5p and was confirmed to negatively modulate miR-424-5p expression. Moreover, overexpression of miR-424-5p partially suppressed the previously high cell viability, migration, and invasion, and activated EMT resulted from upregulation of CDKN2B-AS1, while silencing of miR-424-5p elevated the cellular processes inhibited by silencing the expression of CDKN2B-AS1. Conclusion: The present study revealed that high-expressed CDKN2B-AS1 may associate with the progression of HCC by affecting the cell viability, migration, invasion, and EMT of HCC cells by negatively regulating miR-424-5p.

引用

页码：6807 / 6819

页数：13

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