Comparison of differentiation markers between normal and two squamous cell carcinoma cell lines in culture

Gasparoni, A; Fonzi, L; Schneider, Galen B.; Wertz, Philip W.; Johnson, Georgia K.; Squier, Christopher A.

doi:10.1016/j.archoralbio.2004.02.010

Cited by 21 publications

(15 citation statements)

References 44 publications

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“…Although activating mutations in the ␤-catenin pathway are only found in a subset of hLSCC, [33][34][35] nuclear localization of ␤-catenin and hence increased transcriptional activity are regularly found at the invasive front of hLSCC ( Figure 5). Nuclear ␤-catenin increased with tumor progression, which was reported also for carcinoma of other origin, and to be independent of mutational activation.…”

Section: Discussionmentioning

confidence: 99%

Sonic Hedgehog Acts as a Negative Regulator of β-Catenin Signaling in the Adult Tongue Epithelium

Schneider

Schänzer

Czupalla

et al. 2010

The American Journal of Pathology

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Wnt/␤-catenin signaling has been implicated in taste papilla development; however , its role in epithelial maintenance and tumor progression in the adult tongue remains elusive. We show Wnt/␤-catenin pathway activation in reporter mice and by nuclear ␤-catenin staining in the epithelium and taste papilla of adult mouse and human tongues. ␤-Catenin activation in APC min/؉ mice , which carry a mutation in adenomatous poliposis coli (APC), up-regulates Sonic hedgehog (Shh) and Jagged-2 (JAG2) in the tongue epithelium without formation of squamous cell carcinoma (SCC). We demonstrate that Shh suppresses ␤-catenin transcriptional activity in a signaling-dependent manner in vitro and in vivo. A similar regulation and function was observed for JAG2, suggesting that both pathways negatively regulate ␤-catenin, thereby preventing SCC formation in the tongue. This was supported by reduced nuclear ␤-catenin in the tongue epithelium of Patched ؉/؊ mice , exhibiting dominant active Shh signaling. At the invasive front of human tongue cancer , nuclear ␤-catenin and Shh were increased , suggesting their participation in tumor progression. Interestingly , Shh but not JAG2 was able to reduce ␤-catenin signaling in SCC cells , arguing for a partial loss of negative feedback on ␤-catenin transcription in tongue cancer. We show for the first time that the putative Wnt/␤-catenin targets Shh and JAG2 control ␤-catenin signaling in the adult tongue epithelium, a function that is partially lost in lingual SCC. (Am J

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Section: Discussionmentioning

confidence: 99%

Sonic Hedgehog Acts as a Negative Regulator of β-Catenin Signaling in the Adult Tongue Epithelium

Schneider

Schänzer

Czupalla

et al. 2010

The American Journal of Pathology

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“…The epithelial cells used included a well-differentiated squamous cell carcinoma of the ventral tongue (cell line SCC15) (25) known to express high levels of E-cadherin (14) and were obtained from D. Wong (University of California at Los Angeles). SCC15 cells were maintained in keratinocyte serumfree medium (KSFM) (Invitrogen, Carlsbad, CA) supplemented with 0.4 mM CaCl 2 , 0.1 ng/ml epidermal growth factor, 50 g/ml bovine pituitary extract (Invitrogen, Carlsbad, CA), and antibiotics (100 U/ml penicillin and 100 g/ml streptomycin).…”

Section: Vol 75 2007 C Albicans Degrades E-cadherin 2127mentioning

confidence: 99%

Mucosal Tissue Invasion by Candida albicans Is Associated with E-Cadherin Degradation, Mediated by Transcription Factor Rim101p and Protease Sap5p

et al. 2007

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The ability of Candida albicans to invade mucosal tissues is a major virulence determinant of this organism; however, the mechanism of invasion is not understood in detail. Proteolytic breakdown of E-cadherin, the major protein in epithelial cell junctions, has been proposed as a mechanism of invasion of certain bacteria in the oral mucosa. The objectives of this study were (i) to assess whether C. albicans degrades E-cadherin expressed by oral epithelial cells in vitro; (ii) to compare the abilities of strains with different invasive potentials to degrade this protein; and (iii) to investigate fungal virulence factors responsible for E-cadherin degradation. We found that while E-cadherin gene expression was not altered, E-cadherin was proteolytically degraded during the interaction of oral epithelial cells with C. albicans. Moreover, C. albicans-mediated degradation of E-cadherin was completely inhibited in the presence of protease inhibitors. Using a three-dimensional model of the human oral mucosa, we found that E-cadherin was degraded in localized areas of tissue invasion by C. albicans. An invasion-deficient rim101 ؊ /rim101 ؊ strain was deficient in degradation of E-cadherin, and this finding suggested that proteases may depend on Rim101p for expression. Indeed, reverse transcription-PCR data indicated that expression of the SAP4, SAP5, and SAP6 genes is severely reduced in the rim101 ؊ /rim101 ؊ mutant. These SAP genes are functional Rim101p targets, because engineered expression of SAP5 in the rim101 ؊ /rim101 ؊ strain restored Ecadherin degradation and invasion in the mucosal model. Our data support the hypothesis that there is a mechanism by which C. albicans invades mucosal tissues by promoting the proteolytic degradation of E-cadherin in epithelial adherens junctions.

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“…Human Cell Lines and Culture Conditions SCC25 and OSC2 (OSCC), and DOK (dysplastic oral keratinocytes), and A818-6 (Human Pancreatic Adenocarcinoma) human cell lines have been published [15][16][17][18] and were initially obtained from American Type Culture Collection. The human oral keratinocyte (HOK) whole lysate was purchased from ScienCell TM Research Laboratories (cat.…”

Section: Discussionmentioning

confidence: 99%

Expression of p8 in Human Oral Squamous Cell Carcinoma

Bingham

Dickinson

Cray³

et al. 2014

Head and Neck Pathol

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The present study investigated the expression of p8, a transcription factor upregulated in some human cancers, in oral squamous cell carcinomas (OSCCs). Immunohistochemical analysis of p8 expression was carried out on 20 archived surgical specimens of human OSCCs, and expression correlated with clinical outcome parameters in a retrospective study. Expression of p8 in a number of OSCC cell lines also was investigated by western blot and RT-PCR analyses. p8 was expressed in 80 % (16/20) of the samples with levels of expression exhibiting a significant difference (v 2 = 8.352, df = 3, p = 0.039) by patient age. Furthermore, greater levels of p8 immunoreactivity was significantly associated with advanced tumor grade (p = 0.008). p8 also was upregulated in OSCC cell lines. p8 is expressed in a significant proportion of OSCCs, and in human OSCC cell lines, suggesting a potential value of p8 as a diagnostic and/prognostic tool for oral cancers.

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Comparison of differentiation markers between normal and two squamous cell carcinoma cell lines in culture

Cited by 21 publications

References 44 publications

Sonic Hedgehog Acts as a Negative Regulator of β-Catenin Signaling in the Adult Tongue Epithelium

Sonic Hedgehog Acts as a Negative Regulator of β-Catenin Signaling in the Adult Tongue Epithelium

Mucosal Tissue Invasion by Candida albicans Is Associated with E-Cadherin Degradation, Mediated by Transcription Factor Rim101p and Protease Sap5p

Expression of p8 in Human Oral Squamous Cell Carcinoma

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