LncRNA KCNQ1OT1 Promotes the Development and Progression of Esophageal Squamous Cell Carcinoma via microRNA-125a-5p/STAT3 Axis

Abstract

Background: The crucial role of Long non-coding RNAs (lncRNAs) in the progression of diverse tumors has been reported, including esophageal squamous cell carcinoma (ESCC). Nonetheless, the mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in ESCC is rarely reported. Methods: KCNQ1OT1, miR-125a-5p and Signal transduction and transcriptional activator 3 (STAT3) expression levels in ESCC tissues and cells were examined by qRT-PCR (quantitative real-time polymerase chain reaction). Additionally, Western blot was employed to examine STAT3 protein expression in ESCC cells. The biological functions of KCNQ1OT1, miR-125a-5p and STAT3 in ESCC cells were examined by Cell Counting Kit-8 (CCK-8), EdU (5-ethynyl-2’-deoxyuridine), and Transwell assays. Bioinformatics and dual-luciferase reporter experiments were applied to explore the regulatory mechanisms among KCNQ1OT1, miR-125a-5p and STAT3. Results: KCNQ1OT1 and STAT3 were abnormally up-regulated in ESCC tissues, while miR-125a-5p was abnormally down-regulated. Silencing of KCNQ1OT1 remarkably suppressed the proliferation, migration, and invasion of ESCC cells. MiR-326 inhibition markedly counteracted the tumor-suppressive effect of KCNQ1OT1 silencing on ESCC cells. Moreover, KCNQ1OT1 competitively bound with miR-125a-5p to repress the degradation of STAT3. Conclusions: The findings of this work imply that KCNQ1OT1 is implicated in ESCC progression through modulating miR-125a-5p/STAT3 axis and indicate that KCNQ1OT1 may be a promising biomarker and therapeutic target for ESCC.