LncRNA SLC16A1‐AS1 contributes to the progression of hepatocellular carcinoma cells by modulating miR‐411/MITD1 axis

BACKGROUND: Hepatocellular carcinoma (HCC) is a common malignancy with high morbidity. The current study aimed to explore the molecular mechanism of lncRNA SLC16A1‐AS1 in the tumorigenesis of HCC. MATERIAL AND METHODS: The expression of SLC16A1‐AS1 and miR‐411 was examined in clinical HCC tissues. HCC cell lines Hep3B and Huh‐7 were employed and transfected with si‐SLC16A1‐AS1. The correlation between SLC16A1‐AS1 and miR‐411 was verified by luciferase reporter assay. Cell viability was detected by CCK‐8 assay. Cell migration and invasion capacity were examined by transwell assay. The protein level of MITD1 was analyzed by western blotting. RESULTS: The expression of SLC16A1‐AS1 markedly increased in HCC tissues and cell lines. Subsequent studies identified SLC16A1‐AS1 as a downstream target of miR‐411. In addition, SLC16A1‐AS1 knockdown and miR‐411 overexpression significantly stagnated the progression of HCC cells. SLC16A1‐AS1 knockdown also downregulated MITD1 levels. CONCLUSION: Our findings showed that SLC16A1‐AS1 was overexpressed in HCC cells and tissues. SLC16A1‐AS1 promoted the malignant characteristics of HCC cells and acted as an oncogene. Its regulatory effect may be associated with miR‐411/MITD1 axis. Therefore, SLC16A1‐AS1 has the potential to be used as a biomarker or therapeutic target for the treatment of HCC.