Effects of lncRNA ANRIL on proliferation and apoptosis of oral squamous cell carcinoma cells by regulating TGF-β/Smad pathway.

Abstract

To investigate the role of the long non-coding ribonucleic acid (lncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) in the proliferation and apoptosis of the oral squamous cell carcinoma (OSCC) cells by regulating the transforming growth factor-beta (TGF-β)/Smad pathway. Human OSCC cells were cultured, and then transfected with small interfering (si)-ANRIL to inhibit the lncRNA ANRIL and ANRIL-OE to overexpress the lncRNA ANRIL. Next, the flow cytometry was carried out to detect the apoptosis rate, the proliferation was determined via methyl thiazolyl tetrazolium (MTT) assay, and the changes in the protein level were detected through Western blotting (WB). The lncRNA ANRIL was highly expressed in the tissues and serum of patients. The proliferation ability of the cells transfected with si-ANRIL was significantly reduced, while that of the cells transfected with ANRIL-OE was overtly increased. The apoptosis rate was (9.21±5.22)%, (22.3±1.34)%, and (13.21±6.22)% in lncRNA ANRIL-OE group, si-ANRIL group and control group, respectively. The protein expression level of the apoptotic protein active caspase-3 was lowered after the treatment with ANRIL-OE, and the key molecules of the TGF-β/Smad pathway were notably down-regulated after inhibiting ANRIL with si-ANRIL. The lncRNA ANRIL regulates the TGF-β/Smad signaling pathway to promote the proliferation and suppress the apoptosis of OSCC cells.