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
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.
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.
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.