Junquan Weng

Peri-implant tissue inflammation is an inflammatory injury that occurs in the soft and hard tissues surrounding the implant and is the main cause of short- or long-term failure of implant prosthetic restorations, which is compounded by bone loss and bone destruction in the alveolar bone of diabetes patients with peri-implantitis. However, the mechanisms underlying the persistence of diabetic peri-implantitis, as well as the essential connections and key molecules that regulate its start and progression, remain unknown. In this study, we discovered that M1 macrophage polarization was abnormally enhanced in diabetic peri-implantitis and influenced the osteogenic differentiation of mesenchymal stem cells. RNA sequencing revealed that ALKBH5 expression was abnormally reduced in diabetic peri-implantitis. Further mechanism study showed that ALKBH5 and its mediated m⁶A can influence osteogenic differentiation, which in turn influences the persistence of diabetic peri-implantitis. Our findings present a new mechanism for the suppression of osteoblast development in diabetic peri-implantitis and a new treatment strategy to promote anabolism by inhibiting ALKBH5.

Background. YTH domain containing 1 (YTHDC1), an N6-methyladenosine (m6A) modification reading protein, plays a key role in regulating RNA translation and degradation. However, the role of YTHDC1 in head and neck squamous cell carcinoma (HNSCC) cancer stem cells remains largely unknown. This study is aimed at investigating the role of YTHDC1 in HNSCC and exploring its role in regulating cancer stem cells. Methods. RNA sequencing was used to detect differentially expressed genes (DEGs) between SCC9 spheres and SCC9 cells and to uncover molecular pathways and target molecules associated with CSCs. We detected YTHDC1 expression in The Cancer Genome Atlas (TCGA) database data and clinical samples. Subsequently, YTHDC1 gene suppression assays were performed in HNSCC cell lines to investigate the effect of YTHDC1 on tumor cell stemness maintenance, proliferation, and migration capacity. To further confirm the role of YTHDC1 in regulating cancer stem cells in HNSCC, we analyzed online HNSCC single-cell transcriptomic data to investigate YTHDC1 expression patterns at the single-cell level and the correlation of these levels with the expression of stem cell markers. Results. YTHDC1 expression levels were significantly upregulated in SCC9 spheres, and YTHDC1 was aberrantly expressed in HNSCC tumor tissues. The increased YTHDC1 expression was closely correlated with the clinical characteristics of HNSCC patients. YTHDC1 regulates the malignant phenotype of HNSCC in both in vivo and in vitro studies. Further single-cell transcriptomic data analysis revealed that YTHDC1 positively correlated with malignant epithelial cell stemness capacity at the single-cell level, and that YTHDC1 was involved in regulating stemness maintenance in HNSCC. Conclusions. These findings suggest that YTHDC1 may serve as a biomarker for stem maintenance and malignant progression in HNSCC, providing new insights into the treatment of cancer.

Background. Transforming growth factor β₁-activated kinase 1 binding protein 2 (TAB2) mediates a variety of biological processes through activated nuclear factor κ-light-chain-enhancer of activated B cell (NF-κB) signaling pathways. TAB2 has been reported to be upregulated in a variety of tumors. However, little is known about its potential role in oral squamous cell carcinoma (OSCC). Material and Methods. Patients clinicopathological and transcription data were obtained from The Cancer Genome Atlas (TCGA) database. Immunohistochemistry staining was used to determine TAB2 expression in OSCC tissues (IHC). The expression of TAB2 in OSCC cell lines was detected by western blotting. The CCK-8 test and flow cytometry assay were utilized to evaluate cell proliferation, apoptosis, and cell cycle in OSCC cell lines. Enrichment analysis and identification of predicted signaling pathways were performed by Gene Ontology and KEGG analysis. Finally, the expression of downstream signal molecules was performed using western blotting to validate the mechanism investigations. Results. TAB2 expression level was aberrantly upregulated in OSCC patients. TAB2 expression was shown to be inversely associated to prognosis. The phenotypic of OSCC cells was considerably impacted by TAB2. OSCC cells with deleted TAB2 exhibit decreased proliferation and increased apoptosis. Additionally, OSCC progression is aided by TAB2 overexpression. Further mechanism studies showed that TAB2 could regulate the progression of OSCC by mediating the upregulation of EMT and PI3K-AKT signaling pathways. Conclusion. This study sheds light on the carcinogenic role of TAB2 in OSCC and provides a potential therapeutic strategy.