Long Noncoding RNA MIR100HG Knockdown Attenuates Hepatocellular Carcinoma Progression by Regulating MicroRNA-146b-5p/Chromobox 6

Fushun Li; Xianghua Sun; Qing Liu; Xilu Liu; Jia Zhang

doi:10.1155/2021/6832518

Long Noncoding RNA MIR100HG Knockdown Attenuates Hepatocellular Carcinoma Progression by Regulating MicroRNA-146b-5p/Chromobox 6

Gastroenterol Res Pract. 2021 Jul 30:2021:6832518. doi: 10.1155/2021/6832518. eCollection 2021.

Authors

Fushun Li¹, Xianghua Sun¹, Qing Liu¹, Xilu Liu¹, Jia Zhang²

Affiliations

¹ Department of Hepatobiliary Surgery, Wei Fang Yi Du Central Hospital, No. 4318, South Linglong Mountain Road, Qingzhou County, Weifang City, Shandong Province 262500, China.
² Health Care Department I, Weifang People's Hospital, No. 151, Guangwen Street, Kuiwen District, Weifang City, Shandong Province 261041, China.

Abstract

Purpose: 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.

Materials and methods: 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.

Results: 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.

Conclusions: 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.