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Jian Sun,Lijun Liu,Huilian Zou,Wei Yu 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.10
Purpose: Hepatocellular carcinoma (HCC) is the most common malignant tumor of liver cells. Researchers have reported thatcancer susceptibility candidate 2 (CASC2), a long non-coding RNA, is down-regulated in various cancers, including HCC. Ourstudy aimed to investigate the molecular mechanism(s) of CASC2 in HCC. Materials and Methods: Real-time quantitative PCR (RT-qPCR) was used to analyze the expression of CASC2 and miR-183 inHCC tissues and cells. The viability of HCC SMMC-7721 and Huh-7 cells was detected through MTT assay. Colony formation assaywas performed to assess the colony formation ability of HCC cells. The migration and invasion abilities of HCC cells were evaluatedby Transwell assay. Western blot was conducted to examine levels of key Wnt/β-catenin signaling pathway factors, C-myc, cyclinD,survivin, and β-catenin. The interaction between CASC2 and miR-183 was affirmed by bioinformatics analysis andluciferase reporter assay. Results: CASC2 was down-regulated in HCC tissues and cell lines, while miR-183 was up-regulated. The expression of miR-183was negatively correlated with CASC2 expression in HCC tissues. Overexpression of CASC2 inhibited cell viability, colony formation,migration, and invasion in HCC cells, as well as Wnt/β-catenin signaling pathway activity. miR-183 was a downstream targetof CASC2 and negatively regulated by CASC2. Introduction of miR-183 rescued CASC2-induced suppressive effects on HCC cellviability, colony formation, migration, and invasion and Wnt/β-catenin signaling. Conclusion: CASC2 inhibited cell viability and the colony formation, migration, and invasion abilities of HCC cells by directlydownregulating miR-183 through inactivation of the Wnt/β-catenin signaling pathway.