Increasing evidence has shown that aberrant miRNAs contribute to the development and progression of human melanoma. Previous studies have shown that miR-125b functions as a suppressor in malignant melanoma. However, the molecular function and mechanism by which miR-125b influences melanoma growth and invasion are still unclear. In this study, we aimed to investigate the role of miR-125b in melanoma progression and metastasis. We found that miR-125b expression is significantly downregulated in primary melanoma, and an even greater downregulation was observed in metastatic invasion. Restored expression of miR-125b in melanoma suppressed cell proliferation and invasion both in vitro and in vivo. Furthermore, our findings demonstrate that upregulating miR-125b significantly inhibits malignant phenotypes by repressing the expression of integrin alpha9 (ITGA9). Finally, our data reveal that upregulated expression of ITGA9 in melanoma tissues is inversely associated with miR-125b levels. Together, our results demonstrate that upregulation of ITGA9 in response to the decrease in miR-125b in metastatic melanoma is responsible for melanoma tumor cell migration and invasion.
Background Mena, a cytoskeletal regulatory protein, is involved in actin-based regulation of cell motility and adhesion, and contributes to tumor invasion and metastasis. However, the role of Mena in oral squamous cell carcinoma remains unclear. This is the first research focusing on the prognostic value of Mena in OSCC. In this study, we aimed to investigate the correlation between Mena expression and clinicopathological significance, as well as prognostic value in OSCC. Methods Mena gene expression profiles of OSCC and normal tissues were collected from Oncomine, TCGA, and GEO databases. Biological function was analyzed through GO, KEGG and GSEA enrichment. Further, the expression level of Mena and tumor-related markers in 151 OSCC specimens was examined by IHC staining based on tissue microarray. Kaplan-Meier analysis was used to assess the prognostic performance of Mena in OSCC. Result Mena was generally upregulation in various malignancies, especially OSCC. The functional analyses indicated that Mena was involved in the assembly and regulation of actin, cell movement, and EMT. IHC staining revealed that high expression of Mena in OSCC was correlated with Lymphatic metastasis, TNM stage, E-cadherin, Vimentin, and MMP-2, but insignificantly Ki67. Kaplan-Meier analysis demonstrated that elevated expression of Mena was significantly associated with poor overall survival and disease-free survival of OSCC patients. Conclusion Mena could be a novel biomarker for predicting the prognosis of OSCC patients, which supports a theoretical basis for developing molecular target therapy.
Aim The aim of this clinical trial was to assess the impact of autologous concentrated growth factor (CGF) as a socket-filling material and its ridge preservation properties following the lower third molar extraction. Materials and methods A total of 60 sides of 30 participants who had completely symmetrical bilateral impacted lower third molars were enrolled. The primary outcome variables of the study were bone height and width, bone density, and socket surface area in the coronal section. Cone beam computed tomography images were obtained immediately after surgery and three months after surgery as a temporal measure. Follow-up data were compared to the baseline using paired and unpaired t -tests. Results CGF sites had higher values in height and width when compared to control sites (Buccal wall 32.9 ± 3.5 vs 29.4 ± 4.3 mm, Lingual wall 25.4 ± 3.5 vs 23.1 ± 4 mm, and Alveolar bone width 21.07 ± 1.55vs19.53 ± 1.90 mm, respectively). Bone density showed significantly higher values in CGF sites than in control sites (Coronal half 200 ± 127.3 vs -84.1 ± 121.3 and Apical half 406.5 ± 103 vs 64.2 ± 158.6, respectively). There was a significant difference between both sites in the reduction of the periodontal pockets. Conclusion CGF application following surgical extraction provides an easy, low-cost, and efficient option for alveolar ridge preservation. Thus, the use of CGF by dentists during dental extractions may be encouraged, particularly when alveolar ridge preservation is required. Clinical trial registration TCTR identification, TCTR20221028003.
Abstract Background The surgical extraction of impacted third molars is one of the most common procedures in oral and maxillofacial surgery, which associated with several postoperative complications. The aim of this clinical trial was to estimate the implication of concentrated growth factor (CGF) on postoperative sequelae after the completely impacted lower third molar extraction. Materials and methods A total of 74 sides of 37 participants who had completely bilateral impacted lower third molars were enrolled in this split-mouth, randomized single‑blind, clinical trial. Surgical extraction was undertaken on both sides of the mandible. Randomization was achieved by opaque, sealed envelopes. The postoperative outcomes including wound healing, swelling and pain were clinically assessed at different-time intervals(1st, 3rd and 7th days). A p-value < 0.05 was considered statistically significant. Results The wound healing index was significantly better in the test sides (P = 0.001). Regarding the facial swelling, the test sides had significantly less values than the control sides, particularly on the 1st (1.01 ± .57 vs. 1.55 ± .56) and 3rd days (1.42 ± 0.8 vs. 2.63 ± 1.2) postoperatively. Nonetheless, the swelling was disappeared within the 7th day in both sides. The pain scores of visual analog scale were no a statistically significant difference between both sides on the 1st day, meanwhile, the pain scores were significantly lower in the test sides compared with the control sides, especially on the 3rd (P = 0.001) and 7th days (P < 0.001) postoperatively. Conclusion The application of CGF following the surgical extraction of lower third molar has accelerated the healing of soft tissues as well as reduced postoperative sequelae such as swelling and pain. Therefore, the CGF could be promoted among clinicians during the lower third molar surgical extraction. Trial registration : This study was registered with the TCTR identification number TCTR20210325002 on 25/03/2021 at Thai Clinical Trials Register-Medical Research Foundation of Thailand (MRF). Also it was ethically approved from the institutional ethics committee at the Hospital of Stomatology, Xian Jiaotong University, Xian, China (No: 032), and has been conducted in accordance to the guidelines of the declaration of Helsinki. Written informed consent was obtained from all participants in the study.
Neutrophil elastase (NE) plays a pivotal role in inflammation. However, the mechanism underlying NE-mediated inflammation in obesity remains unclear. Here, we report that NE activates protease-activated receptor-2 (PAR2), stimulates actin filament (F-actin) formation, decreases intercellular junction molecule VE-cadherin expression, and increases the permeability of human arterial endothelial cells (hECs). NE also prompts degradation of VE-cadherin and its binding proteins p120- and β-catenins via MG132-sensitive proteasomes. NE stimulates phosphorylation of myosin light-chain (MLC) and its regulator myosin phosphatase target subunit-1 (MYPT1), a target of Rho kinase (ROCK). Inhibitors of PAR2 and ROCK prohibit NE-induced F-actin formation, MLC phosphorylation, and VE-cadherin reduction in hECs, and impede monocyte transmigration through hEC monolayer pretreated with either neutrophils or NE. Further, administration of an NE inhibitor GW311616A significantly attenuates vascular leakage, leukocyte infiltration, and the expression of proinflammatory cytokines in the white adipose tissue from high-fat diet (HFD)-induced obese mice. Likewise, NE-deficient mice are resistant to HFD-induced vascular leakage in the heart. Together, NE regulates actomyosin cytoskeleton activity and VE-cadherin expression by activating PAR2 signaling in the endothelial cells, leading to increased vascular permeability and leukocyte extravasation. Hence, inhibition of NE is a potential approach to mitigate vascular injury and leukocyte infiltration in obesity-related systemic inflammation.
Abstract Background Clinical instructional strategies and the climate in which teaching and learning take place have a significant impact on the quality of dental education. Therefore, this study aimed to evaluate the impact of early microsurgery training on the skills of dental intern students who are planning to join an oral and maxillofacial surgical field (DIS) as compared with junior residents within an oral and maxillofacial surgery department who had no microsurgery experience (JR). Methods A total of 100 trainees, 70 were DIS, while the other 30 were JR. The average age was 23.87 ± 2.05 years for DIS group and 31.05 ± 3.06 for JR group. All trainees attended a microsurgical course (theoretical and practical parts) for seven days within a Microvascular Laboratory for Research and Education of a university-affiliated tertiary hospital. Two blinded examiners had assessed the performance of trainees independently using a specific scoring system. The independent sample t-test was used to compare the effect of microsurgery training between DIS and JR groups. The significance level was set at 0.05. Results The DIS group had showed higher attendance rate than JR group (p < 0.01), with a lower absence score in DIS than JR groups (0.33 ± 0.58 vs. 2.47 ± 1.36). The total score of the theoretical test was significantly different between both groups (p < 0.01). In this context, the DIS group had revealed higher total score than JR group (15.06 ± 1.92 vs. 12.73 ± 2.49). In term of tissue preservation, there was a significant difference between both groups, with the DIS had better performance score than JR (1.49 ± 0.51 vs. 0.93 ± 0.59). Further, the practical exam score was significantly higher in DIS group than JR group (p < 0.01). Conclusion Overall, the performance of dental intern students was favourably compared with junior residents in most aspects. Therefore, it is promising and essential for dental colleges to add a microsurgery course to the curriculum of dental intern students who plan to specialize in oral and maxillofacial surgery.
Objectives: Head and neck squamous cell carcinoma (HNSCC) is the most common malignancy of the head and neck. However, the molecular mechanisms governing the development of HNSCC have not been fully elucidated. Materials and Methods: Differentially expressed genes (DEGs) were screened out from The Cancer Genome Atlas (TCGA) and GSE23036 datasets. Weighted gene coexpression network analysis (WGCNA) was used to reveal the correlations among genes and to search for significantly correlated gene modules. The expression levels of genes in HNSCC and normal samples according to antibody-based detected methods was assessed by utilizing the Human Protein Atlas (HPA). The impact of the selected hub genes on the prognosis of HNSCC patients was assessed by analysing immunohistochemistry (IHC) and immunofluorescence (IF) expression levels and clinical data. Results: Twenty-four genes positively correlated with tumour status and 15 genes negatively correlated with tumour status were screened out by WGCNA. PLAU and LAMC2 were associated with a poor prognosis in patients with HNSCC and were finally screened out and verified by GEPIA and HPA database analysis. Immunohistochemistry of samples collected from 175 patients with HNSCC and subsequent statistical analysis also showed that PLAU and LAMC2 were associated with a poor prognosis in patients with HNSCC, and the levels of these two factors were positively correlated. The expression and co-localization of PLAU and LAMC2 in HNSCC tissues were confirmed by double immunofluorescence labeling. Conclusions: There was a positive correlation between PLAU and LAMC2 expression in HNSCC samples, and PLAU and LAMC2 might be independent prognostic biomarkers for HNSCC.
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