BACKGROUND: Double-stranded RNA-specific adenosine deaminase 1 (ADAR1) binds to double-stranded RNA and catalyzes the deamination of adenosine (A) to inosine (I). The functional mechanism of ADAR1 in non-small cell lung cancer (NSCLC) remains incompletely understood. This study aimed to investigate the prognostic significance of ADAR1 in NSCLC and to elucidate its potential role in regulating tumor cell proliferation and migration. METHODS: Data from The Cancer Genome Atlas (TCGA) and cBioPortal were analyzed to assess the correlation between high ADAR1 expression and clinicopathological features as well as prognosis in lung cancer. We performed Western blot (WB), cell proliferation assays, Transwell invasion/migration assays, and nude mouse xenograft modeling to examine the phenotypic changes and molecular mechanisms induced by ADAR1 knockdown. Furthermore, the ADAR1 p150 overexpression model was utilized to validate the proposed mechanism. RESULTS: ADAR1 expression was significantly elevated in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) tissues compared with adjacent non-tumor tissues (LUAD: P=3.70×10-15, LUSC: P=0.016). High ADAR1 expression was associated with poor prognosis (LUAD: P=2.03×10-2, LUSC: P=2.81×10-2) and distant metastasis (P=0.003). Gene Set Enrichment Analysis (GSEA) indicated that elevated ADAR1 was associated with mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway activation, matrix metalloproteinase-9 (MMP-9) expression, and cell adhesion. ADAR1 and MMP-9 levels showed a strongly positive correlation (P=6.45×10-34) in 10 lung cancer cell lines, highest in H1581. Knockdown of ADAR1 in H1581 cells induced a rounded cellular morphology with reduced pseudopodia. Concomitantly, it suppressed cell proliferation, invasion, migration, and in vivo tumorigenesis. It also suppressed ERK phosphorylation and downregulated cellular Finkel-Biskis-Jinkins murine osteosarcoma viral oncogene homolog (c-FOS), MMP-9, N-cadherin, and Vimentin. Conversely, ADAR1 p150 overexpression in PC9 cells enhanced ERK phosphorylation and increased c-FOS and MMP-9 expression. CONCLUSIONS High ADAR1 expression is closely associated with poor prognosis and distant metastasis in NSCLC patients. Mechanistically, ADAR1 may promote proliferation, invasion, migration, and tumorigenesis in lung cancer cells via the ERK/c-FOS/MMP-9 axis.
Humans ; Lung Neoplasms/physiopathology* ; Adenosine Deaminase/genetics* ; Matrix Metalloproteinase 9/genetics* ; Cell Proliferation ; Carcinoma, Non-Small-Cell Lung/physiopathology* ; Cell Movement ; Animals ; Mice ; RNA-Binding Proteins/genetics* ; Female ; Male ; Cell Line, Tumor ; Proto-Oncogene Proteins c-fos/genetics* ; Middle Aged ; MAP Kinase Signaling System ; Gene Expression Regulation, Neoplastic ; Mice, Nude ; Extracellular Signal-Regulated MAP Kinases/genetics*

Objective To analyse the location of the mandibular canal,providing the theoretical basis for implanting and bone grafting. Methods Mandibular data of 83 Chinese people obtained by cone-beam computed tomography examination were collected. Results The distance from the mandibular canal to mandibular buccal wall was (5.32 ± 1.29)~(7.24 ± 1.29) mm. And the average distance from mandibular canal to mandibular lingual wall or inferior margin were respectively (3.43 ± .99) ~ (3.93 ± 1.17) mm and (8.81 ± 1.90) ~ (10.02 ± 2.19) mm. Significant differences between males and females were found in groups. The anterior loop was observed in 70.9%of all sides. The accessory mental foramen was observed in 10.84% of all sides. Conclusion For the remarkable mutation of the location of the mandibular canal in Chinese people, clinicians should be careful before implant or bone surgery procedures to minimize the risk of inferior alveolar nerve injury.

Objective To study the pre-and post-surgical orthodontic treatment methods of patients with skeletal malocclusion treated through combined orthodontic-orthognathic surgery,and to set some guidance for the future clinical Work.Methods Twenty-five skeletal malocclusion patients in our clinic aged from 17 to 36 were treated by presurgical orthodontic treatment,orthognathic surgery and postsurgical ortho dontic treatment.Presurgical orthodontic treatment included alignment of dental arches,leveling of arches,elimination of rotations,coordination of the arches,and decompensation of anterior and posterior teeth.The postsurgical orthodontic treatment included closing residual spacing,final tooth alignment,maximum interdigitation,finalizing torque,artistic positioning,ideal overjet/overbite relationship and establishment of correct root parallelism.Results The duration of presurgical orthodontic treatment was 14.41 months on average(2～23 months),and the postsurgical orthodontic treatment time was 6.94 months on average(1.5～13.5 months).The duration for the whole active treatment was 21.35 months on average(7～35 months).The maxilla was moved back on an average 5.00 mm in maxillary protrusion cases.The mandible was moved anteriorly on an average 7.25 mm in mandibular retrusion cases.The mandible was moved back on an average 6.55 mm in mandibular protrusion cases.The chin was moved anteriorly on an average 5.33 nan in retrusion of chin cases.Conclusions Pre-and post-surgical orthodontic treatments are important procedures to the surgical treatment for skeletal malocclusion and basic needs to obtain successful treatment results.