Lehong Qiu1, Linlin Zheng2, Chengwen Gan1, Wei Deng1, Ying Sun1, Tao Wang1. 1. Department of Stomatology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, China. 2. Department of Central Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University Haikou, Hainan, China.
Abstract
BACKGROUND: Circular RNAs (circRNAs) are related to oral squamous cell carcinoma (OSCC) progression. circRNA bicaudal D cargo adaptor 2 (circBICD2) has been reported to be abnormally expressed in OSCC. However, the function and mechanism of this circRNA in OSCC progression remain largely unknown. METHODS: circBICD2, microRNA-149-5p (miR-149-5p), and insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) abundances were examined via quantitative reverse transcription polymerase chain reaction or Western blot. The function of circBICD2 was investigated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, flow cytometry, wound healing, transwell, specific kits, Western blot, and xenograft analyses. Dual-luciferase reporter analysis and RNA immunoprecipitation were carried out to analyze the binding interaction. RESULTS: circBICD2 expression was enhanced in OSCC tissues and cells. circBICD2 silence suppressed OSCC cell proliferation, migration, invasion, and glutaminolysis and facilitated apoptosis. miR-149-5p was targeted via circBICD2 and decreased in OSCC tissues and cells. miR-149-5p knockdown attenuated silence of circBICD2 on the influence of OSCC cell proliferation, apoptosis, migration, invasion, and glutaminolysis. IGF2BP1 was targeted via miR-149-5p, and circBICD2 could regulate IGF2BP1 via miR-149-5p. IGF2BP1 interference constrained OSCC cell proliferation, migration, invasion, and glutaminolysis and promoted apoptosis. circBICD2 silence reduced OSCC cell growth in xenograft model. CONCLUSION: circBICD2 knockdown repressed OSCC cell proliferation, migration, invasion, and glutaminolysis and increased apoptosis via modulating miR-149-5p/IGF2BP1 axis, which might act as a potential target for OSCC treatment.
BACKGROUND: Circular RNAs (circRNAs) are related to oral squamous cell carcinoma (OSCC) progression. circRNA bicaudal D cargo adaptor 2 (circBICD2) has been reported to be abnormally expressed in OSCC. However, the function and mechanism of this circRNA in OSCC progression remain largely unknown. METHODS: circBICD2, microRNA-149-5p (miR-149-5p), and insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) abundances were examined via quantitative reverse transcription polymerase chain reaction or Western blot. The function of circBICD2 was investigated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, flow cytometry, wound healing, transwell, specific kits, Western blot, and xenograft analyses. Dual-luciferase reporter analysis and RNA immunoprecipitation were carried out to analyze the binding interaction. RESULTS: circBICD2 expression was enhanced in OSCC tissues and cells. circBICD2 silence suppressed OSCC cell proliferation, migration, invasion, and glutaminolysis and facilitated apoptosis. miR-149-5p was targeted via circBICD2 and decreased in OSCC tissues and cells. miR-149-5p knockdown attenuated silence of circBICD2 on the influence of OSCC cell proliferation, apoptosis, migration, invasion, and glutaminolysis. IGF2BP1 was targeted via miR-149-5p, and circBICD2 could regulate IGF2BP1 via miR-149-5p. IGF2BP1 interference constrained OSCC cell proliferation, migration, invasion, and glutaminolysis and promoted apoptosis. circBICD2 silence reduced OSCC cell growth in xenograft model. CONCLUSION: circBICD2 knockdown repressed OSCC cell proliferation, migration, invasion, and glutaminolysis and increased apoptosis via modulating miR-149-5p/IGF2BP1 axis, which might act as a potential target for OSCC treatment.