Li Fushun, Sun Xianghua, Liu Qing, Liu Xilu, Zhang Jia
Department of Hepatobiliary Surgery, Wei Fang Yi Du Central Hospital, No. 4318, South Linglong Mountain Road, Qingzhou County, Weifang City, Shandong Province 262500, China.
Health Care Department I, Weifang People's Hospital, No. 151, Guangwen Street, Kuiwen District, Weifang City, Shandong Province 261041, China.
Gastroenterol Res Pract. 2021 Jul 30;2021:6832518. doi: 10.1155/2021/6832518. eCollection 2021.
Hepatocellular carcinoma (HCC) accounts for approximately ninety percent of primary liver cancer. This study attempted to investigate the effects of the long noncoding RNA MIR100HG (MIR100HG) in HCC and the underlying molecular mechanism.
qRT-PCR was implemented to analyze the expression of MIR100HG, microRNA-146b-5p (miR-146b-5p), and Chromobox 6 (CBX6). The correlation between MIR100HG and clinicopathological features of HCC patients was assessed. Additionally, the effects of MIR100HG knockdown on HCC cell viability, migration, and invasion were explored. The interactions among MIR100HG, miR-146b-5p, and CBX6 were confirmed. Furthermore, rescue experiments were conducted to investigate whether MIR100HG knockdown modulates HCC cell behaviors through modulating the miR-146b-5p/CBX6 axis.
The expression of MIR100HG and CBX6 was enhanced, while miR-146b-5p was inhibited in HCC cells. High MIR100HG expression was positively associated with the TNM tumor stage and Edmondson-Steiner grading in HCC patients. MIR100HG knockdown considerably reduced the HCC cell viability, migration, and invasion. In addition, MIR100HG directly targeted miR-146b-5p, and miR-146b-5p directly targeted CBX6 in HCC cells. Moreover, miR-146b-5p suppression or CBX6 elevation evidently rescued the suppressed viability, migration, and invasion of HCC cells caused by MIR100HG knockdown.
Knockdown of MIR100HG inhibited the viability, migration, and invasion of HCC cells by targeting the miR-146b-5p/CBX6 axis, offering a potential therapeutic target for HCC therapy.
肝细胞癌（HCC）约占原发性肝癌的90%。本研究旨在探讨长链非编码RNA MIR100HG（MIR100HG）在HCC中的作用及其潜在分子机制。
采用qRT-PCR分析MIR100HG、微小RNA-146b-5p（miR-146b-5p）和染色质盒蛋白6（CBX6）的表达。评估MIR100HG与HCC患者临床病理特征之间的相关性。此外，探讨了敲低MIR100HG对HCC细胞活力、迁移和侵袭的影响。证实了MIR100HG、miR-146b-5p和CBX6之间的相互作用。此外，进行了挽救实验，以研究敲低MIR100HG是否通过调节miR-146b-5p/CBX6轴来调节HCC细胞行为。
HCC细胞中MIR100HG和CBX6的表达增强，而miR-146b-5p受到抑制。HCC患者中高MIR100HG表达与TNM肿瘤分期和Edmondson-Steiner分级呈正相关。敲低MIR100HG显著降低了HCC细胞的活力、迁移和侵袭能力。此外，在HCC细胞中，MIR100HG直接靶向miR-146b-5p，miR-146b-5p直接靶向CBX6。此外，抑制miR-146b-5p或升高CBX6明显挽救了敲低MIR100HG导致的HCC细胞活力、迁移和侵袭能力的抑制。
敲低MIR100HG通过靶向miR-146b-5p/CBX6轴抑制HCC细胞的活力、迁移和侵袭，为HCC治疗提供了一个潜在的治疗靶点。
