Shen Xinying, Li Yong, He Fan, Kong Jian
Department of Interventional Radiology, Shenzhen People's Hospital, Shenzhen, Guangdong, People's Republic of China.
Cancer Manag Res. 2020 Aug 4;12:6807-6819. doi: 10.2147/CMAR.S240000. eCollection 2020.
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.
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.
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 up-regulation of CDKN2B-AS1, while silencing of miR-424-5p elevated the cellular processes inhibited by silencing the expression of CDKN2B-AS1.
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.
肝细胞癌（HCC）导致高死亡率和转移。在本研究中，研究了长链非编码RNA（lncRNA）CDKN2B-AS1对HCC进展的影响。
检测HCC癌组织及癌旁组织和HCC细胞中lncRNA CDKN2B-AS1的表达。随后，在HCC细胞中过表达和沉默CDKN2B-AS1，通过细胞计数试剂盒-8（CCK-8）、伤口愈合、Transwell和蛋白质印迹法观察CDKN2B-AS1对HCC细胞活力、迁移、侵袭和上皮-间质转化（EMT）的影响。预测并验证CDKN2B-AS1的靶基因是miR-424-5p，测定其在CDKN2B-AS1表达上调或下调的HCC细胞中的表达。此外，通过上调或下调miR-424-5p以及过表达或沉默CDKN2B-AS1，研究miR-424-5p对HCC细胞活力、迁移、侵袭和EMT的影响。
CDKN2B-AS1在HCC组织和细胞中表达增加。沉默CDKN2B-AS1可抑制细胞活力、迁移、侵袭和EMT，而过表达CDKN2B-AS1则产生相反的结果。此外，预测并验证CDKN2B-AS1靶向miR-424-5p，并证实其对miR-424-5p表达具有负调控作用。此外，miR-424-5p的过表达部分抑制了先前因CDKN2B-AS1上调而导致的高细胞活力、迁移和侵袭，并激活了EMT，而沉默miR-424-5p则提高了因沉默CDKN2B-AS1表达而受到抑制的细胞进程。
本研究表明，高表达的CDKN2B-AS1可能通过负调控miR-424-5p影响HCC细胞的活力、迁移、侵袭和EMT，从而与HCC的进展相关。
