Expression Pattern and Value of Brain-Derived Neurotrophic Factor in Periodontitis.

BACKGROUND: Periodontitis is a common human disease with an increasing incidence. Brain-derived neurotrophic factor (BDNF) is known to play a crucial role in the regeneration of periodontal tissue; however, the expression, methylation level, molecular function, and clinical value of BDNF in periodontitis require further investigation. This study aimed to investigate the expression and potential functions of BDNF in periodontitis. METHODS: RNA expression and methylation data were obtained from the Gene Expression Omnibus (GEO) database, and the expression and methylation levels of BDNF were compared between periodontitis and normal tissues. In addition, bioinformatics analysis was performed to investigate the downstream molecular functions of BDNF. Finally, Reverse transcription Quantitative real-time polymerase chain reaction was performed to determine the level of BDNF expression in periodontitis and normal tissues. RESULTS: GEO database analysis revealed that BDNF was hypermethylated in periodontitis tissues and that its expression was downregulated. Reverse transcription Quantitative real-time polymerase chain reaction confirmed that BDNF expression was downregulated in periodontitis tissues. Several genes that interact with BDNF were determined using a protein-protein interaction network. Functional analysis of BDNF revealed that it was enriched in the Gene Ontology terms cytoplasmic dynein complex, glutathione transferase activity, and glycoside metabolic process. Kyoto Encyclopedia of Genes and Genomes analysis suggested that BDNF was associated with the mechanistic target of rapamycin signaling pathway, fatty acid metabolism, the Janus kinase-signal transducer and activator of transcription signaling pathway, glutathione metabolism, and others. Furthermore, the level of BDNF expression was correlated with the immune infiltration degree of B cells and CD4+ T cells. CONCLUSIONS: This study shown that BDNF was hypermethylated and downregulated in periodontitis tissues, which could be a biomarker and treatment target of periodontitis.

RELA promotes the progression of oral squamous cell carcinoma via TFAP2A-Wnt/ß-catenin signaling.

Oral squamous cell carcinoma (OSCC) has emerged as the most prevailing oral malignancy worldwide, characterized by cervical solid lymph node metastasis and strong local invasiveness. Overexpression of Transcription Factor AP-2 alpha (TFAP2A) is observed in a significant proportion of OSCC cases. In this study, we aimed to elucidate the function of TFAP2A in the progression of OSCC and the related molecular signaling pathways. The role of RELA was predicted using bioinformatics analysis. The mRNA abundances of RELA, TFAP2A, and ß-catenin were assessed by Western blot and quantitative real-timePCR. The relationship between RELA, TFAP2A, and ß-catenin and their correlation with clinicopathological characteristics of OSCC was evaluated. The target of RELA and TFAP2A was identified by the chromatin immunoprecipitation as well as luciferase reporter assay. The colony formation assay and MTS assay were performed to determine the proliferative level of OSCC cells. OSCC cell motility was determined by Transwell assay and wound-healing assay. The protein expressions of epithelial-mesenchymal transition-associated factors were evaluated by Western blot. The expressions of RELA and TFAP2A were elevated in OSCC, and their expressions displayed a positive correlation. The expression levels of RELA and TFAP2A were found to be associated with TNM staging and lymphatic metastasis of OSCC patients. RELA upregulation promoted OSCC progression, as manifested by increased levels of proliferation, invasion, and migration of OSCC cells. We also demonstrated that RELA was directly bound to the promoter of TFAP2A transcription, which activated multiple malignant and metastatic phenotypes. Furthermore, TFAP2A activated the Wnt/ß-catenin signaling by targeting the promoter regions of ß-catenin. The study found that RELA is critical for promoting the progression of OSCC via the RELA-TFAP2A-Wnt/ß-catenin signaling pathway. The RELA-TFAP2A-Wnt/ß-catenin signaling pathway is a potential target for reducing the aggressiveness of OSCC.

X-Ray Cephalometric Analysis of the Effects of Angle Class II and III Malocclusion on the Upper Airway Width and Hyoid Position between Parents and Children of Uygur Nationality.

Objective: The objective of this paper is to analyze the effect of angle class II and III malocclusion on the sagittal diameter of the upper airway between parents and children of Uygur nationality and to compare the degree of influence. Methods: 29 Uygur adolescents with malocclusion and their fathers (mothers) were selected as our subjects via X-ray cephalometric radiograph to analyze the difference between the upper airway sagittal dimension and normal occlusion and compare the influence of malocclusion on the upper airway between parents and children. Results: Compared with normal group, the vertical distance from the hyoid point to orbital-ear plane (H-FH) and vertical distance from hyoid point to the mandibular plane (H-MP) in angle class II malocclusion elevated signally, while the vertical distance from hyoid point to anterior cervical plane (H-VL), PNS-UPW, H-FH, and H-MP decreased significantly; compared with normal group: the distance between the posterior nasal spine and the upper pharynx wall (PNS-UPW), H-FH, and H-MP in angle class III malocclusion visually reduced, while PAS, and horizontal distance from the hyoid point and center point of sella turcica to orbital-ear foot (H-S), increased markedly. The impact of class II malocclusion on parents' U-MPM was greater than their children. Conclusion: The oropharyngeal space of upper airway becomes smaller and hyoid shifts downwards due to class II malocclusion. Class III malocclusion results in decreased nasopharyngeal gap with hyoid to shift upward. The influence of class II malocclusion on the upper pharyngeal tract of parents was greater than their children.

The role of long non-coding RNA LINC01296 in oral squamous cell carcinoma: a study based on bioinformatics analysis and in vitro validation.

Background: Oral squamous cell carcinoma (OSCC) is a common malignancy in the oral cavity that represents a significant global health problem. Multivariate analysis has shown that long non-coding RNA LINC01296 plays an important role in cancer biology. However, the functions of LINC01296 in OSCC are still unknown. Methods: The RNA profiles and clinicopathological information of OSCC patients and healthy subjects were downloaded. The expression level and prognostic value of LINC01296 were assessed. The functions and pathways of LINC01296were explored using the Gene Set Enrichment Analysis (GSEA) and functional analysis. The expression of LINC01296 in OSCC tissues and cell lines was determined by RT-qPCR. MTS assay was used to evaluate cell growth. The migration and invasion capacities of cells were assessed by wound healing assay and Transwell assay. Results: LINC01296 was overexpressed in the TCGA-OSCC datasets. High LINC01296expression was strongly correlated with poor outcomes of OSCC patients. LINC01296 was overexpressed in OSCC tissues compared with para-carcinoma tissues. Moreover, the expression of linc01296 was higher in CAL-27, HSC-2, and SCC-25 cells than in normal human oral keratinocytes (NHOKs). Functional analysis suggested that LINC01296might be involved in the regulation of the Wnt and MAPK signaling pathways. Additionally, LINC01296 deficiency suppressed the growth, migration, and invasion of OSCC cells, whereas overexpression of TFAP2A-AS1 cause opposite results. Conclusion: Our study showed that LINC01296 promoted OSCC cell growth, migration, and invasion, suggesting that LINC01296 might be a potential therapeutic target for OSCC.

MicroRNA-222-3p participates in the development of oral squamous cell carcinoma by targeting CDKN1B.

OBJECTIVE: The aim of this study was to explore the potential role and regulatory mechanism of microRNA (miR)-222-3p in oral squamous cell carcinoma (OSCC). METHODS: The expression level and prognostic significance of miR-222-3p was detected in OSCC tissues. CCK-8, transwell, and flow cytometry assays were used to explore the effect of miR-222-3p on cell proliferation, migration, invasion, and apoptosis. The influence of miR-222-3p on cyclin-dependent kinase inhibitor 1B (CDKN1B) expression was evaluated by luciferase assays, real-time polymerase chain reaction, and Western blot. RESULTS: We found that miR-222-3p was overexpressed in OSCC tissues, comparing with normal tissues. Kaplan-Meier curves showed that OSCC patients with high expression of miR-222-3p (P = .003) showed worse overall survival than those patients with low expression of miR-222-3p. Multivariate analysis showed that miR-222-3p (P = .037) expression was an independent prognostic factor of OSCC patients. miR-222-3p promoted cell proliferation, migration and invasion and induced the apoptosis of SCC-15 and Tca-83 cells. Furthermore, luciferase reporter assays indicated that CDKN1B is targeted by miR-222-3p in OSCC cells. Overexpression of CDKN1B inhibited OSCC cell proliferation, migration, and invasion and promoted cell apoptosis rate. CONCLUSIONS: miR-222-3p affects OSCC cell proliferation, migration, invasion, and apoptosis through targeting CDKN1B, and may be a potential prognostic biomarker for OSCC patients.