Oral Cancer

Thus, we deduce that the NNMT inhibitors affect mitochondrial activity indirectly via NNMT. It is concluded that NNMT is a potential drug target for oral cancer.

OSMF-derived OSCC exhibits a distinct transcriptomic landscape compared with de novo OSCC, characterized by altered epithelial differentiation, immune modulation, and activation of developmental pathways. The observed gene dysregulation findings establish that OSCC developing in the background of OSMF is molecularly distinct from de novo OSCC, underscoring the biological impact of the pre-existing fibrotic milieu on tumor transcriptional architecture.

Objectives: pH-responsive zeolite imidazolate framework-8 (ZIF-8) enables selective release of 5-fluorouracil (5-FU) within the acidic tumor microenvironment...Apoptosis-related signaling was also elevated in SCC7 cells compared with DPSCs. ZIF-8 at 100 μg/mL selectively inhibits SCC7 growth while sparing OMSC viability and apoptosis.

Proteomic analysis indicated that miR-185 EV suppressed OSCC progression by downregulating interleukin-1β (IL-1β), consequently inhibiting the NF-κB signaling pathway. The findings demonstrate the successful development of the miR-185 EV-loaded gelatin/lignin hydrogel that represents an effective nanomedicine platform for intraoral drug delivery, providing a promising strategy for the clinical treatment of OSCC.

In this experimental model, experimental periodontitis was accompanied by concurrent increases in both local and systemic ANGPTL2 expression and accelerated growth of colorectal tumors. These findings suggest a potential association between periodontal inflammation, increased ANGPTL2 levels, and colorectal tumor progression.

Benign salivary gland tumors represent a valuable model for studying malignant transformation in head and neck oncology. Interpreting shared molecular and microenvironmental pathways may facilitate the identification of novel biomarkers and support the development of personalized diagnostic and therapeutic approaches for OSCC.

LINC01106 exerts oncogenic effects via the miR-449a/MYC axis and may serve as a therapeutic target in OSCC.

The remaining, ubiquitination-independent internalization required EGFR kinase activity, was highly clathrin-dependent, and was significantly impaired by depletion of the AP-2 clathrin adaptor complex. Interestingly, inhibition of CBLs and EGFR endocytosis by NX-1013 did not affect major downstream signaling pathways in human oral squamous cell carcinoma cells, with the exception of Rac1 activation and EGFR-dependent cell migration, both of which were suppressed.

While informative, cfDNA quantification alone offers limited prognostic reliability, reinforcing the need for a multidimensional approach that includes genomic and clinical evaluation. Overall, this study supports the potential of liquid biopsy as a real-time, non-invasive tool for molecular monitoring and personalized management of OSCC patients.

Importantly, these potent anticancer effects were conserved in another OSCC cell line (YD‑10B) and, were validated in vivo, where PP1 suppressed tumor growth in a zebrafish xenograft model. Collectively, these findings suggest that PP1 exerts strong anticancer effects on human oral cancer by simultaneously inhibiting Src activity and disrupting a network of associated oncogenic pathways (EGFR, STAT‑3, PKB and ERK‑1/2).

The results demonstrate that acid stress skews normal OECs towards pro-inflammatory and pro-oncogenic phenotypes when faced with concomitant microbial ligand challenge and provide key molecular clues to OEC survival strategies with potential implications for elucidating the early molecular events in the development of epithelial dysplasia. Acute acid exposure reduces survival of OECsA subpopulation of OECs is resistant to acid-mediated cell loss and undergo morphometric changes consistent with epithelial-mesenchymal transitionConcurrent acid stress and TLR stimulation modulates transcription of immune and metabolic genes in OECsAcid stress increases TGF-β1 protein production of OECs following TLR agonist stimulation.