Wnt/β‐catenin signaling is an evolutionarily conserved pathway and plays a crucial role in regulating cancer cell proliferation and tumorigenesis. However, the molecular mechanism behind the Wnt/β‐catenin signaling-mediated carcinogenesis and apoptosis resistance in oral squamous cell carcinoma is not well characterized so far. In the present study, we have investigated the effect of β‐catenin depletion of the perversely activated Wnt/β-catenin signaling pathway on apoptosis resistance and tumorigenesis of the human OSCC cell line SCC-55. RT-PCR and western blot analysis demonstrated that the Wnt/β-catenin signaling pathway and its downstream targets such as DKK1 and AXIN2 are aberrantly activated in SCC-55 cells. Furthermore, upon silencing (RNA interference) of β‐catenin in SCC-55, cells became more sensitive toward the chemotherapeutic drugs and thus resulted in apoptotic cell death. Meanwhile, flow cytometry analysis confirmed the enhanced apoptosis and activation of caspases in β‐catenin RNAi cells. Besides ensuing β-catenin–siRNA transfection, the cell proliferation and cancer colony generating efficiencies are significantly impeded compared to the non-transfected cells. Furthermore, the tumorigenicity was inhibited by the downregulation of OCT-4 in β‐catenin-silenced SCC-55 cells. Altogether, Wnt/β‐catenin signaling could potentially target anti-cancer drugs to induce apoptosis and achieve a better clinical outcome.

ObjectivePeriodontal disease (PD) is viewed today as multifactorial problems initiated and sustained by bacteria but significantly modified by the body’s response to bacterial plaque. Recent studies have suggested that gene polymorphisms could be involved in the pathophysiology of periodontitis. This study aimed to investigate a possible correlation of the polymorphisms of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) with PD.MethodsThe genotypes of ICAM-1 and VCAM-1 were initially determined in PD patients using denaturing high performance liquid chromatography (DHPLC). ELISA was then conducted to measure ICAM-1 and VCAM-1 protein levels. Next, the association of ICAM-1/VCAM-1 genotype distribution and expression with clinical indicators and severity of PD was analyzed.ResultsPD patients contained increased levels of hemoglobin A1c (HbA1c), total cholesterol (TC), triglyceride (TG), and low-density lipoprotein (LDL), increased ICAM-1 and VCAM-1 protein levels, and decreased high-density lipoprotein (HDL) level. The GG genotype and G allele at ICAM-1 rs5498, as well as the AG and GG genotypes and G allele at VCAM-1 rs3181092 may reduce PD risk.ConclusionTo sum up, the overexpressed ICAM-1 and VCA M-1 as well as A allele of ICAM-1 rs5498 and VCAM-1 rs3181092 is associated with the onset of PD.

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