ABSTRACT
BACKGROUND/AIMS: Emerging evidence suggests that the propagation of oral squamous cell carcinoma (OSCC) is influenced by the abnormal expression of microRNAs (miRNAs). This study aimed to characterize the involvement of miR-182-5p in OSCC by targeting the calcium/ calmodulin-dependent protein kinase II inhibitor CAMK2N1. METHODS: miR-182-5p expression was quantified in OSCC tissues and cell lines with reverse transcription polymerase chain reaction (RT-PCR). Cell colony formation, Cell Counting Kit-8 (CCK-8), Ki-67, and nude mouse xenograft assays were used to characterize the role of miR-182-5p in the proliferation of OSCC. A miR-182-5p target gene was identified with western blotting, RT-PCR, and luciferase activity assays. OSCC patient survival based on CAMK2N1 expression was also analyzed. RESULTS: miR-182-5p was up-regulated in in vitro cell lines and in vivo clinical OSCC samples. CCK-8, colony formation, and Ki-67 assays revealed that miR-182-5p promoted the growth and proliferation of OSCC cells. miR-182-5p directly targeted CAMK2N1, as evidenced by luciferase assays and target prediction algorithms. CAMK2N1 operated as a tumor suppressor gene in patients with OSCC. Down-regulating miR-182-5p expression in the CAL-27 cell line restored CAMK2N1-mediated OSCC cell proliferation. miR-182-5p expression inhibited the activation of AKT, ERK1/2, and NF-κB. Mice injected with CAL-27 cells transfected with miR-182-5p-inhibitor demonstrated a significant increase in tumor size and weight and increased CAMK2N1 mRNA and protein expression compared with the miR-negative control group. CONCLUSION: The miR-182-5p-CAMK2N1 pathway can be potentially targeted to regulate the proliferation of OSCC cells.
Subject(s)
Carcinoma, Squamous Cell/pathology , MicroRNAs/metabolism , Mouth Neoplasms/pathology , Proteins/metabolism , Animals , Antagomirs/metabolism , Antagomirs/therapeutic use , Carcinoma, Squamous Cell/drug therapy , Carcinoma, Squamous Cell/metabolism , Cell Line, Tumor , Cell Proliferation , Humans , Kaplan-Meier Estimate , Male , Mice , Mice, Inbred BALB C , Mice, Nude , MicroRNAs/antagonists & inhibitors , MicroRNAs/genetics , Mitogen-Activated Protein Kinase 1/metabolism , Mitogen-Activated Protein Kinase 3/metabolism , Mouth Neoplasms/drug therapy , Mouth Neoplasms/metabolism , NF-kappa B/metabolism , Proteins/antagonists & inhibitors , Proteins/genetics , Proto-Oncogene Proteins c-akt/metabolism , RNA Interference , RNA, Small Interfering/metabolismABSTRACT
OBJECTIVE: To introduce the clinical application and curative effect of lateral lag screw technique in fixing condylar intracapsular sagittal fractures. METHODS: Thirteen condyles with intracapsular sagittal fracture of 11 cases were fixed using lateral lag screw technique. Curative effects were observed by clinical and radiological follow-up for 6 approximately 30 months (mean 12 months) postoperatively. RESULTS: The favorable results were obtained in all cases. All patients were satisfied with the clinical results. slight malocclusion existed in 2 cases. Radiological abnormalities were seen in 3 cases by CT scanning, but without any obvious function disturbances. CONCLUSIONS: Lateral lag screw technique is a simple and effective treatment in fixing intracapsular sagittal condylar fractures.
