Long non-coding RNA ST8SIA6-AS1 promotes the migration and invasion of hypoxia-treated hepatocellular carcinoma cells through the miR-338/MEPCE axis

Hepatocellular carcinoma (HCC) is one of the most prevalent types of cancer worldwide. Long non-coding RNAs (lncRNAs) have been reported to frequently participate in the carcinogenesis and development of various types of cancer, including HCC. However, the molecular mechanisms of lncRNA ST8SIA6-AS1 in HCC remain poorly understood. The present study performed bioinformatics analysis, in addition to using reverse transcription-quantitative PCR (RT-qPCR), nuclear-cytoplasmic fractionation, RNA immunoprecipitation, and Transwell, wound healing, and dual-luciferase reporter assays, to determine the biological role and regulatory mechanisms of ST8SIA6-AS1 in HCC. The results revealed that the expression levels of ST8SIA6-AS1 were upregulated in HCC tissues and cell lines, which were associated with a poor prognosis. Moreover, the genetic knockdown of ST8SIA6-AS1 inhibited the hypoxia-induced HCC cell migration and invasion. Additionally, microRNA (miR)-338, which exhibited downregulated expression levels in HCC tissues and cell lines, was discovered to bind with ST8SIA6-AS1. The inhibition of miR-338 partially reversed the inhibitory effects of ST8SIA6-AS1-knockdown on the migration and invasion of HCC cells under hypoxia. Subsequently, methylphosphate capping enzyme (MEPCE) was identified to be targeted and negatively regulated by miR-338. Notably, the overexpression of MEPCE recovered the inhibitory influence over the migratory and invasive abilities of hypoxia-treated HCC cells promoted by ST8SIA6-AS1 inhibition. In conclusion, the findings of the present study suggest that lncRNA ST8SIA6-AS1 may promote the migration and invasion of hypoxia-induced HCC cells via the miR-338/MEPCE axis, indicating a potential diagnostic or therapeutic marker for HCC treatment.

Automated summary

This study revealed that ST8SIA6-AS1 was upregulated in HCC tissues and cells, promoting the migration and invasion of hypoxia-induced HCC cells through the miR-338/MEPCE axis.