• Asian Pacific Journal of Cancer Prevention
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• v.15 no.2
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• pp.871-876
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• 2014

Objective: Desmogleins (DSGs) are major members among the desmosomal cadherins critically involved in cell-cell adhesion and the maintenance of normal tissue architecture in epithelia. Reports exploring links of DSG family member expression with cancers are few and vary. The aim of this study was to investigate the ratio of DSG2 and DSG3 mRNA expression in esophageal squamous cell carcinoma (ESCC) tissue to normal tissue (T/N ratio) and evaluate correlations with clinical parameters. Methods: The mRNA expression of DSGs, as well as ${\gamma}$-catenin and desmoplakin, was detected by real-time quantitative RT-PCR in 85 cases of ESCC tissue specimens. Results: The expression level of DSG3 mRNA was significantly higher than that of DSG2 in ESCC specimens (p=0.000). DSG3 mRNA expression highly correlated with histological grade (p=0.009), whereas that of DSG2 did not significantly relate to any clinicopathologic parameter. Kaplan-Meier survival analysis showed that only DSG3 expression had an impact on the survival curve, with negative DSG3 expression indicating worse survival (p=0.038). Multivariate Cox regression analysis demonstrated DSG3 to be an independent prognostic factor for survival. Furthermore, correlation analysis demonstrated the mRNA level of DSG3 to highly correlate with those of ${\gamma}$-catenin and desmoplakin in ESCC samples (p=0.000), implying that the expression of desmosomal components might be regulated by the same upstream regulatory molecules. Conclusions: Our findings suggest that DSG3 may be involved in the progression of ESCC and serve as a prognostic marker, while expression of DSG2 cannot be used as a predictor of ESCC patient outcome.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.31 no.5
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• pp.414-418
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• 2009

Pemphigus vulgaris is a chronic autoimmune intraepithelial blistering disease with oral mucosal manifestations that very often precede the skin lesions. The vesicles or bullae are produced by an acantholytic process, detachment of differentiating keratinocytes from one another in the epithelial stratum spino sum or spinous cell layer. The pathogenesis of this disease is initially manifested by IgG(mainly) binding to desmosome(desmoglein 3 or 1) in the intercellular spaces of epithelium. This autoantibody binding caused the release of a plasminogen activator(a proteolytic enzyme) from keratinocytes. This ultimately results in cell to cell separation. The mainstay therapy of pemphigus vulgaris is systemic corticosteroids and immunosuppressive agents to eliminate the pathogenic autoantibodies from circulation. A 41-year old woman presented with a 1.5 year history of oral ulceration. There were no lesions on the skin or other mucosal sites. Histology and immunostaining were consistent with pemphigus vulgaris. Control of oral ulceration and normal oral function were achieved after systemic corticosteroids and immunosuppressive agents were instituted.

• Animal cells and systems
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• v.14 no.4
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• pp.261-266
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• 2010

PC12 cells were differentiated into the cells of chromaffin phenotype by butyrate treatment. Cells were aggregated and formed tight cell adhesion. To investigate the molecular change in this differentiation, we examined expression levels of cell adhesion proteins and extracellular proteins during butyrate induced-differentiation of PC12 cells. Integrin ${\beta}1$, integrin ${\alpha}7$, E cadherin, VCAM, collagen-I, fibronectin, desmoglein and connexin were increased during differentiation. The levels of clusterin and secreted clusterin were also increased. These increased levels of cell adhesion proteins and extracellular proteins appear to induce cell aggregation and tight cell adhesion. The levels of p21, p27 and p16 were increased probably because of differentiation-related growth arrest during differentiation. Prolonged incubation of butyrate up to 1 day was required for differentiation. Signal transduction pathways for this differentiatiom could not be identified since various inhibitors had no effect. The results showed that butyrateinduced differentiation of PC12 cells to chromaffin cells involves tight cell adhesion and induction of extracellular proteins and cell adhesion proteins.