Cancer Management and Research (Aug 2020)
Circ_0015756 Aggravates Hepatocellular Carcinoma Development by Regulating FGFR1 via Sponging miR-610
Abstract
Weisheng Guo,1 Lin Zhao,1 Guangya Wei,1 Peng Liu,1 Yu Zhang,1 Liran Fu2 1Department of Hepatobiliary Surgery, Henan Province Hospital of Traditional Chinese Medicine, The Second Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, Henan 450002, People’s Republic of China; 2Department of Traditional Chinese Medicine, People’s Hospital of Zhengzhou, Zhengzhou, Henan 450000, People’s Republic of ChinaCorrespondence: Liran FuDepartment of Traditional Chinese Medicine, People’s Hospital of Zhengzhou, Zhengzhou, Henan 450000, People’s Republic of ChinaTel +86- 15837117112Email [email protected]: Hepatocellular carcinoma (HCC) is the leading threat of cancer-related death in humans. Increasing studies show that circular RNAs (circRNAs) are important indicators in cancer diagnosis and prognosis. This study intended to explore the function and mechanism of circ_0015756 in HCC, providing the additional opinion for HCC treatment.Materials and Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to detect the expression of circ_0015756 and miR-610. Cell viability was assessed by cell counting kit-8 (CCK-8) assay, and colony formation capacity was ascertained by colony formation assay. Cell migration and invasion were monitored by transwell assay. Cell cycle progression and apoptosis were analyzed by flow cytometry assay. Circ_0015756 oncogenicity was determined by Xenograft models. The targets of circ_0015756 and miR-610 were predicted by bioinformatics tools and validated using RNA pull-down, RNA immunoprecipitation (RIP) and dual-luciferase reporter assays. The expression level of fibroblast growth factor receptor 1 (FGFR1) was measured by Western blot.Results: The expression of circ_0015756 was increased in HCC tissues, serums and cells. Circ_0015756 downregulation impaired HCC cell viability, colony formation capacity, invasion and migration, induced cell cycle arrest and apoptosis, and inhibited tumor growth in vivo. MiR-610 was ensured as a target of circ_0015756, and miR-610 absence reversed the effects of circ_0015756 downregulation. Further, FGFR1 was targeted by miR-610, and FGFR1 overexpression overturned the effects of miR-610 restoration in HCC cells. Circ_0015756 could regulate FGFR1 expression by targeting miR-610.Conclusion: Circ_0015756 played its tumorigenic properties in HCC by activating FGFR1 via sponging miR-610, and circ_0015756 was expected to be a vital indicator in HCC diagnosis and treatment.Keywords: circ_0015756, miR-610, FGFR1, HCC
