Desmoglein 3 is overexpressed in inverted papilloma and squamous cell carcinoma of sinonasal cavity

Huang, Chi‐Che; Lee, Ta‐Jen; Chang, Phei‐Lang; Lee, Yun‐Shien; Chuang, Chi‐Cheng; Jhang, You-Jia; Chen, Yiwei; Chen, Chiang-Wen; Tsai, Chia-Lung

doi:10.1002/lary.20151

Cited by 30 publications

(28 citation statements)

References 11 publications

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“…5– 7). Such changes are consistent with the observation that in squamous cell carcinoma (head and neck, and lung) and inverted papilloma augmented expression of Dsg3 has been reported [13]–[15], [17], [58]. Our data suggest that Src activation in hDsg3.myc cells was independent of EGFR in our culture conditions, since no changes were detected either in levels of protein expression or in its phosphorylation status [43] (Fig.…”

Section: Discussionsupporting

confidence: 93%

Desmoglein 3, via an Interaction with E-cadherin, Is Associated with Activation of Src

et al. 2010

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BackgroundDesmoglein 3 (Dsg3), a desmosomal adhesion protein, is expressed in basal and immediate suprabasal layers of skin and across the entire stratified squamous epithelium of oral mucosa. However, increasing evidence suggests that the role of Dsg3 may involve more than just cell-cell adhesion.Methodology/Principal FindingsTo determine possible additional roles of Dsg3 during epithelial cell adhesion we used overexpression of full-length human Dsg3 cDNA, and RNAi-mediated knockdown of this molecule in various epithelial cell types. Overexpression of Dsg3 resulted in a reduced level of E-cadherin but a colocalisation with the E-cadherin-catenin complex of the adherens junctions. Concomitantly these transfected cells exhibited marked migratory capacity and the formation of filopodial protrusions. These latter events are consistent with Src activation and, indeed, Src-specific inhibition reversed these phenotypes. Moreover Dsg3 knockdown, which also reversed the decreased level of E-cadherin, partially blocked Src phosphorylation.Conclusions/SignificanceOur data are consistent with the possibility that Dsg3, as an up-stream regulator of Src activity, helps regulate adherens junction formation.

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Section: Discussionsupporting

confidence: 93%

Desmoglein 3, via an Interaction with E-cadherin, Is Associated with Activation of Src

et al. 2010

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“…These structures are essential for maintaining tissue integrity and architecture. Huang et al [40], investigated the role of Desmoglein 3 (DSG3), a 130-kD transmembrane glycoprotein, and found it overexpressed in SNIP and in SNIP with SCC. DSG3 expression might be associated with the architecture transformations of these tumors and its overexpression is correlated with malignant transformation of SNIP.…”

Section: Desmosomesmentioning

confidence: 99%

Malignant transformation of sinonasal inverted papilloma and related genetic alterations: a systematic review

Gioacchini

Bajraktari

et al. 2017

Eur Arch Otorhinolaryngol

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Schneiderian papillomas are uncommon tumors which may develop within the nasal cavity and comprise three well-defined histological types: sinonasal inverted papilloma (SNIP), exophytic papilloma, and oncocytic papilloma. It is well known the rate of Schneiderian papilloma may also present a malignant degeneration and SNIP represents the most important subgroup in consideration of its frequency and malignant propensity. Although HPV infection is always considered the first event favoring the development of SNIP, however, it is not established as an eventual connection between viral actions and malignant transformation. In fact, different molecular mechanisms are suspected to play a crucial role in this process and, currently, many authors agree that only by improving our knowledge about these mechanisms it will be possible to achieve new and effective targeted therapies. So the aim of this study was firstly to systematically review the literature focusing on different biomarkers that could be implicated in the stages of SNIP malignant degeneration. Secondly, a systematic review with meta-analysis was performed to better define the incidence of sinonasal malignancies originating from Schneiderian papilloma (SNIP, exophytic papilloma, and oncocytic papilloma). Twenty-nine studies comprising a total of 3177 patients were statistically analyzed. Results showed a 9% (95% CI = 7-11) overall rate of malignant transformation from Schneiderian papilloma. In conclusion, this analysis confirmed that the potential malignancy of Schneiderian papilloma should not be underestimated. On the other hand, our review showed the paucity of studies investigating the molecular alterations which may be related with the malignant transformation of SNIP.

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“…Other studies report enhanced expression of desmosomal cadherins in cancer (Brennan & Mahoney, 2009;Brown et al, 2014;Chen et al, 2007;De Bruin et al, 1999;Huang et al, 2010;Kurzen et al, 2003;Savci-Heijink et al, 2009). Therefore, both loss and overexpression of desmosomal cadherin expression frequently correlate with advanced tumor grading, increased invasion and metastasis, and/ or poor prognosis/survival.…”

Section: Activation Of Invasion and Metastasismentioning

confidence: 95%

150th Anniversary Series: Desmosomes and the Hallmarks of Cancer

Huber

Petersen

2015

Cell Communication & Adhesion

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Desmosomes represent adhesive, spot-like intercellular junctions that in association with intermediate filaments mechanically link neighboring cells and stabilize tissue architecture. In addition to this structural function, desmosomes also act as signaling platforms involved in the regulation of cell proliferation, differentiation, migration, morphogenesis, and apoptosis. Thus, deregulation of desmosomal proteins has to be considered to contribute to tumorigenesis. Proteolytic fragmentation and downregulation of desmosomal cadherins and plaque proteins by transcriptional or epigenetic mechanisms were observed in different cancer entities suggesting a tumor-suppressive role. However, discrepant data in the literature indicate that context-dependent differences based on alternative intracellular, signal transduction lead to altered outcome. Here, modulation of Wnt/β-catenin signaling by plakoglobin or desmoplakin and of epidermal growth factor receptor signaling appears to be of special relevance. This review summarizes current evidence on how desmosomal proteins participate in carcinogenesis, and depicts the molecular mechanisms involved.

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Desmoglein 3 is overexpressed in inverted papilloma and squamous cell carcinoma of sinonasal cavity

Cited by 30 publications

References 11 publications

Desmoglein 3, via an Interaction with E-cadherin, Is Associated with Activation of Src

Desmoglein 3, via an Interaction with E-cadherin, Is Associated with Activation of Src

Malignant transformation of sinonasal inverted papilloma and related genetic alterations: a systematic review

150th Anniversary Series: Desmosomes and the Hallmarks of Cancer

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