Abstract
The present study investigated the expression profile and the function of RP11-169D4.1 and explored its potential mechanisms in laryngeal squamous cell carcinoma. The biological function of RP11-169D4.1 was examined using the MTT assay, flow cytometric analysis, wound healing and transwell assays. The relationship between RP11-169D4.1 and miR-205-5p was discovered by Argonaute 2 protein immunoprecipitation. The target gene of RP11-169D4.1 was CDH1 which was assessed by Pearson's correlation analysis, RT-PCR and western blot assay. We demonstrated that RP11-169D4.1 expression was markedly decreased in LSCC tissues and cell lines. The overexpression of RP11-169D4.1 inhibited the proliferation, migration and invasion of LSCC cell lines as well as promoted apoptosis. We further verified that miR-205-5p had binding sites with RP11‑169D4.1 and that RP11-169D4.1 could regulate the expression of CDH1. Ectopic transfection of RP11-169D4.1 led to a significant reduction in the downstream signaling molecule AKT in LSCC cells. The long non-coding RNA RP11-169D4.1 may serve as a tumor suppressor and a promising therapeutic target in laryngeal cancer, which could inhibit the process of EMT by regulating CDH1.