RP11-284F21.9 promotes oral squamous cell carcinoma development via the miR-383-5p/MAL2 axis.

Abstract

Increasing evidence suggests that dysregulated long non-coding RNAs (lncRNAs) are involved in tumorigenesis and progression. RP11-284F21.9, one of the temporally expressed S-phase lncRNAs in cancer cells, was recently identified by nascent RNA capture sequencing. Cal-27, Tca8113, SCC-9, HB56, and oral squamous cell carcinoma (OSCC) tissues were used in the experiment. RNA extraction, qRT-PCR, plasmid construction, cell proliferation, EdU labeling, Transwell migration, luciferase reporter, and western blotting were used to investigate the exact role and function of RP11-284F21.9 in cancer. RP11-284F21.9 was upregulated in human OSCC samples and cell lines. RP11-284F21.9 depletion suppressed the proliferation, migration, and invasion of OSCC cell lines. There was interaction between RP11-284F21.9, miR-383-5p, and MAL2. Increased MAL2 and decreased miR-383-5p expression were also detected in OSCC tissues and cell lines. In addition, RP11-284F21.9 knockdown could reduce MAL2 expression, while miR-383-5p inhibitors abolished this repressive effect. RP11-284F21.9 acted as a competing endogenous RNA (ceRNA) of miR-383-5p, leading to MAL2 upregulation, and subsequently promoted OSCC progression. RP11-284F21.9/miR-383-5p represents a novel and potential therapeutic target for the treatment of OSCC.