LncRNA FAM83A-AS1 aggravates the malignant development of esophageal cancer by binding to miR-495-3p.

Abstract

It is of significance to screen out differentially expressed long non-coding RNAs (lncRNAs) that can be utilized as tumor biomarkers in esophageal cancer. This study aims to uncover the effect of lncRNA FAM83A-AS1 on regulating migratory potential in esophageal cancer and the underlying mechanism. Tumor tissues and adjacent normal ones were collected from 62 esophageal cancer patients for detecting FAM83A-AS1 levels. Correlations of FAM83A-AS1 with clinical indexes and overall survival of esophageal cancer patients were analyzed. Thereafter, regulatory effects of FAM83A-AS1 on migratory potential in OE19 and OE33 cells were examined by transwell and wound healing assay. Then, the target genes of FAM83A-AS1 were predicted and functionally analyzed, and a protein interaction network was constructed. Finally, the mechanism of FAM83A-AS1 in regulating the downstream gene miR-495-3p was analyzed through Luciferase assay and rescue experiments. It was found that FAM83A-AS1 was upregulated in esophageal cancer tissues and cell lines. Higher rates of lymphatic and distant metastasis and worse survival were observed in esophageal cancer patients expressing higher level of FAM83A-AS1. Besides, the knockdown of FAM83A-AS1 suppressed migratory potential in OE19 cells, while the overexpression of FAM83A-AS1 yielded the opposite trend in OE33 cells. Moreover, miR-495-3p was indicated to be the target gene binding FAM83A-AS1, and it was lowly expressed in esophageal cancer and negatively regulated by FAM83A-AS1. Furthermore, the overexpression of miR-495-3p partially abolished the regulatory effect of FAM83A-AS1 on migratory potential in esophageal cancer. FAM83A-AS1 is upregulated in esophageal cancer, and it stimulates migratory potential in esophageal cancer by negatively regulating miR-495-3p.