Bioinformatics analysis of CUL2/4A/9 and its function in head and neck squamous cell carcinoma

Introduction: Several previous studies have shown that differential expression of cullin (CUL) family proteins may be involved in mediation of the signal transduction pathways associated with cancer. However, the function of CULs is still unclear in head and neck squamous cell carcinoma (HNSCC). Material and methods: We used The Cancer Genome Atlas (TCGA) database, cBioPortal, Metascape, STRING, Cytoscape, Tumor Immune Estimation Resource (TIMER), Kaplan-Meier plotter, and Tumor Immune System Interaction Database (TISIDB) to access the expression of CULs and the possible correlation with the tumourigenesis, development, prognosis, immunity, and transcriptional level of CULs in HNSCC. Furthermore, real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect messenger ribonucleid acid (mRNA) levels in HNSCC tissues and cell samples. We also explored the cell proliferation and migration separately by CCK8 assay and wound healing assay. Results: The results showed that the expressions of CUL2/4A were upregulated and CUL9 was downregulated in HNSCC patients as compared with normal patients. CUL2/4A/9 were also linked to the clinicopathological features and overall survival of HNSCC in bioinformatics analysis. Moreover, we noticed that CUL2/4A/9 may take part in tumour-specific immune response by modulating the tumour-infiltrating lymphocytes (TILs) and immunomodulators. Lastly, we found that CUL2/4A/9 could promote cellular proliferation and migration. Conclusion: These results suggest that the transcriptional levels of CUL2/4A/9 were upregulated and these genes could affect proliferation and migration of HNSCC cells. Therefore, CUL2/4A/9 could potentially function as novel independent biomarkers in HNSCC patients

Treatment of Gingival Recession with Microinvasive Surgical Technology

Objective. The purpose of this clinical research was to evaluate the result of microinvasive surgical technology: vestibular incision subperiosteal tunnel access (VISTA) and subepithelial connective tissue graft (SCTG) in multiple gingival recession. Methods. A total of 20 patients with 25 Miller I and 30 Miller III gingival recession teeth were treated with VISTA+SCTG. The data at baseline and 12 months were assessed: probing depth (PD), clinical attachment loss (CAL), gingival recession depth (RD), gingival recession width (RW), width of keratinized tissue (WKT), and gingival biotype (GB), and percentage of root coverage (RC) and complete root coverage (CRC) were calculated. Results. The average root coverage was 1.52±0.70 mm in Miller I and 0.82±0.79 mm in Miller III. The mean root coverage rate was 99.00%±5.00% in Miller I and 60.73±37.90% in Miller III. The width of clinical attachment loss of keratinized tissue was significantly improved. Conclusions. VISTA and SCTG are effective in the treatment of both Miller class I and III multiple gingival recessions. Gingival increment in Miller class I is better than that in III. It is the same for maxillary and mandibular teeth

Identification of SLC2A3 as a prognostic indicator correlated with the NF-κB/EMT axis and immune response in head and neck squamous cell carcinoma

ABSTRACTSLC2A3 is an important member of the glucose transporter superfamily. It has been recently suggested that upregulation of SLC2A3 is associated with poor survival and acts as a prognostic marker in a variety of tumors. Unfortunately, the prognostic role of SLC2A3 in head and neck squamous cell carcinoma (HNSC) is less known. In the present study, we analyzed SLC2A3 expression in HNSC and its correlation with prognosis using TCGA and GEO databases. The results showed that SLC2A3 mRNA expression was higher in HNSC compared with adjacent normal tissues, which was validated with our 9 pairs of HNSC specimens. Moreover, high SLC2A3 expression predicted poor prognosis in HNSC patients. Mechanistically, GSEA revealed that high expression of SLC2A3 was enriched in epithelial-mesenchymal transition (EMT) and NF-κB signaling. In HNSC cell lines, SLC2A3 knockdown inhibited cell proliferation and migration. In addition, NF-κB P65 and EMT-related gene expression was suppressed upon SLC2A3 knockdown, indicating that SLC2A3 may play a preeminent role in the progression of HNSC through the NF-κB/EMT axis. Meanwhile, the expression of SLC2A3 was negatively correlated with immune cells, suggesting that SLC2A3 may be involved in the immune response in HNSC. The correlation between SLC2A3 expression and drug sensitivity was further assessed. In conclusion, our study demonstrated that SLC2A3 could predict the prognosis of HNSC patients and mediate the progression of HNSC via the NF-κB/EMT axis and immune responses