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The Long Non-Coding RNA CASC2 Suppresses Cell Viability, Migration, and Invasion in Hepatocellular Carcinoma Cells by
Jian Sun1, Lijun Liu1, Huilian Zou2
1Department II of General Surgery, The People's Hospital of Hanchuan, Hanchuan, Hubei, China.
Purpose:
Hepatocellular carcinoma (HCC) is the most common malignant tumor of liver cells. Researchers have reported that cancer susceptibility candidate 2 (CASC2), a long non-coding RNA, is down-regulated in various cancers, including HCC. Our study 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 in HCC tissues and cells. The viability of HCC SMMC-7721 and Huh-7 cells was detected through MTT assay. Colony formation assay was performed to assess the colony formation ability of HCC cells. The migration and invasion abilities of HCC cells were evaluated by 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 and luciferase reporter assay.
Results:
CASC2 was down-regulated in HCC tissues and cell lines, while miR-183 was up-regulated. The expression of miR-183 was 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 target of CASC2 and negatively regulated by CASC2. Introduction of miR-183 rescued CASC2-induced suppressive effects on HCC cell viability, 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 directly downregulating miR-183 through inactivation of the Wnt/β-catenin signaling pathway.
Insights
Cancer susceptibility candidate 2 (CASC2) is reduced in liver cancer. CASC2 inhibits hepatocellular carcinoma (HCC) growth and spread by downregulating miR-183 and the Wnt/β-catenin pathway.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Hepatocellular carcinoma (HCC) is a primary liver cancer.
- Cancer susceptibility candidate 2 (CASC2), a long non-coding RNA, is often downregulated in cancers, including HCC.
Purpose of the Study:
- To investigate the molecular mechanisms of CASC2 in HCC.
- To determine the role of CASC2 in HCC progression and its interaction with miR-183 and the Wnt/β-catenin pathway.
Main Methods:
- Real-time quantitative PCR (RT-qPCR) and Western blot were used to analyze gene and protein expression.
- Cell viability, colony formation, migration, and invasion assays were performed.
- Bioinformatics analysis and luciferase reporter assays confirmed molecular interactions.
Main Results:
- CASC2 expression was decreased, while miR-183 was increased in HCC tissues and cells.
- CASC2 overexpression suppressed HCC cell viability, proliferation, migration, and invasion.
- CASC2 directly downregulated miR-183, inhibiting the Wnt/β-catenin signaling pathway.
Conclusions:
- CASC2 acts as a tumor suppressor in HCC.
- CASC2 inhibits HCC progression by downregulating miR-183 and inactivating the Wnt/β-catenin pathway.
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