KCNQ1OT1 promotes migration and inhibits apoptosis by modulating miR-185-5p/Rab14 axis in oral squamous cell carcinoma.

Long non-coding RNAs (lncRNAs) play essential roles in the regulation of gene transcription in carcinogenesis and metastasis via interacting with microRNA. In this study, we explored the expressions and functions of lncRNA KCNQ1OT1 and miR-185-5p in oral squamous cell carcinoma (OSCC) cells. KCNQ1OT1 expression in OSCC tissues and cells was examined by qRT-PCR. Small interfering RNAs against KCNQ1OT1 (si- KCNQ1OT1) were used to knockdown KCNQ1OT1 in OSCC cells. Cell function was assessed by wound healing assay, transwell assay, and apoptosis detection. The binding region between KCNQ1OT1 and miR-185-5p was confirmed by luciferase assays. MiR-185-5p expression was measured by qRT-PCR. Rab14 was confirmed as a downstream target gene of miR-185-5p by measuring luciferase activities. The protein level of Rab14 in OSCC cells transfected with miR-185-5p or si-KCNQ1OT1 was determined by Western blot. The OSCC cell function and Rab14 expression after co-transfection of si-KCNQ1OT1 and miR-185-5p inhibitor were also examined. KCNQ1OT1 was upregulated in OSCC tissues and cells. KCNQ1OT1 silencing suppressed OSCC cell malignancy and downregulated miR-185-5p level, which showed upregulated expression in OSCC samples. Rab14 as a target gene of miR-185-5p was highly expressed in OSCC. KCNQ1OT1 knockdown impaired the invasion capability of OSCC cells, promoted apoptosis, and suppressed Rab14 expression. The inhibition of miR-185-5p in KCNQ1OT1 silencing cells reversed the suppression of Rab14 and restored the cancerous growth of OSCC cells. These results indicated that KCNQ1OT1 promoted OSCC tumorigenesis via the modulation of miR-185-5p/Rab14 axis, which may serve as a therapeutic target for the treatment of OSCC.