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Background: Chronic hepatitis C virus (HCV) infection is an important risk factor for hepatocellular carcinoma (HCC). EGOT is a long non-coding RNA (lncRNA) induced after HCV infection that increases viral replication by antagonizing the antiviral response. Interestingly, EGOT also acts as a crucial regulator in multiple cancers. However, its role in HCC remains unclear.
Methods: Real-time PCR (RT-PCR) was used to detect the expression of EGOT in HCC samples and cell lines. CCK-8 assay and colony formation assay were performed to evaluate the effect of EGOT on proliferation. Scratch healing assay and transwell assay were used to detect the changes of migration and invasion. Flow cytometry was used to detect the effect of EGOT on apoptosis. Interaction between EGOT and miR-33a-5p was determined by bioinformatics analysis, RT-PCR, and dual-luciferase reporter assay. Western blot was used to confirm that high mobility group protein A2 (HMGA2) could be modulated by EGOT.
Results: Compared with normal liver tissues, the expression level of EGOT in HCC tissues was significantly up-regulated. EGOT markedly regulated viability, migration and invasion of HCC cells. The expression level of EGOT was negatively correlated the expression level of miR-33a-5p. It is also confirmed that EGOT could specifically bind to miR-33a-5p and could reduce its expression, in turn, up-regulate the expression of HMGA2.
Conclusion: Our data imply that EGOT may be a novel therapeutic target for HCC, and highlights the key role of EGOT/miR-33a-5p/HMGA2 in the progression of this deadly disease.
Keywords: HCV, HCC, EGOT, miR-33a-5p, HMGA2