LncRNA FAM83A-AS1 Dives ESCC Progression by Regulating miR-214/CDC25B Axis

Abstract

Background Recently, extensive researches have established that long non-coding RNA (lncRNA) was an important factor that is strongly related to carcinogenesis. However, the function of lncRNAs in esophageal cell squamous carcinoma (ESCC) remains to be explored. In the current study, we assessed the expression pattern and the biological function of FAM83A-AS1 in ESCC. Methods qRT-PCR was used to detect the expression of FAM83A-AS1,miR-214, and CDC25B expression in ESCCtissues and cell lines. Cell counting kit 8 (CCK-8, Transwell, apoptosis, and cell cycle assays were performed to define the function of FAM83A-AS1 in ESCC cell. Furthermore, the regulation of miR-214 by FAM83A-AS1 was defined by qRT- PCR and rescue assays.In addition, the association between CDC25B,miR-214,CDC25B were performed with qRT-PCR.Results: Here we discovered that FAM83A-AS1 was strongly expressed in ESCC tissues. FAM83A-AS1 abundance was associated with TNM stages and the differentiation grade of ESCC patients. The receiver operating characteristic curve (ROC) analysis indicated the high accuracy of FAM83A-AS1 in ESCC diagnosis. Functionally, inhibiting FAM83A-AS1 repressed cell proliferation, migration, and invasion in ESCC. In addition, we found that FAM83A-AS1 accelerated cell cycle and inhibited cell apoptosis. Mechanistically, we found that FAM83A-AS1 regulated miR-214 expression and there was a negative correlation between miR-214 and FAM83A-AS1 in ESCC. Rescue assay indicated that miR-214 could impair the suppressing effect of cell migration induced by FAM83A-AS1 depletion. Furthermore, CDC25B was a direct target of miR-214 and FAM83A-AS1 enhanced CDC25B expression while miR-214 positively CDC25B expression in ESCC. Conclusions Collectively, we concluded that FAM83A-AS1 facilitated ESCC progression by regulating the miR-214/CDC25B axis. Our study showed FAM83A-AS1 may act as a target for ESCC diagnosis and therapy.