L Liu1, S-B Ning, S Fu, Y Mao, M Xiao, B Guo. 1. Department of Oral and Maxillofacial-Head & Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. cycstal2002@12.com.
Abstract
OBJECTIVE: 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. PATIENTS AND METHODS: 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). RESULTS: 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. CONCLUSIONS: The lncRNA ANRIL regulates the TGF-β/Smad signaling pathway to promote the proliferation and suppress the apoptosis of OSCC cells.
OBJECTIVE: 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. PATIENTS AND METHODS: HumanOSCC cells were cultured, and then transfected with small interfering (si)-ANRIL to inhibit the lncRNAANRIL and ANRIL-OE to overexpress the lncRNAANRIL. 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). RESULTS: The lncRNAANRIL 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 lncRNAANRIL-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. CONCLUSIONS: The lncRNAANRIL regulates the TGF-β/Smad signaling pathway to promote the proliferation and suppress the apoptosis of OSCC cells.
Authors: Christian Idel; Julika Ribbat-Idel; Luise Klapper; Rosemarie Krupar; Karl-Ludwig Bruchhage; Eva Dreyer; Dirk Rades; Christina Polasky; Anne Offermann; Jutta Kirfel; Sven Perner; Barbara Wollenberg Journal: Front Oncol Date: 2021-10-28 Impact factor: 6.244