Dickkopf (Dkk)-3 and β-catenin expressions increased in the transition from normal oral mucosal to oral squamous cell carcinoma

Fujii, Michihiko; Katase, Naoki; Lefeuvre, Mathieu; Gündüz, Mehmet; Buery, Rosario Rivera; Tamamura, Ryo; Tsujigiwa, Hidetsugu; Nagatsuka, Hitoshi

doi:10.1007/s10735-011-9357-z

Cited by 34 publications

(32 citation statements)

References 18 publications

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“…The Wnt/β-catenin axis plays a crucial role in tissue homeostasis, regeneration and repair [38], and was therefore investigated in a model of radiation-induced oral mucositis by Zhao et al., who reported on the mucoprotective potential of Wnt activation [39]. Without stimulation, β‑catenin expression, similarly to our results and in good agreement with other publications on normal mucosa [40, 41], remained membrane bound. Irradiation comprised one single high-dose fraction and Zhao et al.…”

Section: Discussionsupporting

confidence: 93%

Upregulated epithelial junction expression represents a novel parameter of the epithelial radiation response to fractionated irradiation in oral mucosa

et al. 2018

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PurposeDuring head and neck cancer treatment, the radiation response of the oral mucosa represents a frequent early side effect. Besides radiation-induced inhibition of proliferation, various other cellular responses occur. The radiation response of adherens and tight junction proteins was so far mostly investigated with large single-dose irradiation protocols, in vivo and in vitro. Therefore, the current study was initiated to investigate the impact of daily fractionated irradiation on the expression of adherens and tight junction proteins in vivo.Materials and methodsFractionation with 5 × 3 Gy/week (days 0–4, 7–11) was given to the snouts of mice. Groups of 5 animals per day were euthanized every second day between day 0 (unirradiated controls) and day 14, and their tongues subjected to histological processing. Adherens junction marker (β-catenin and E‑cadherin) and tight junction marker (claudin-1 and occludin) expression was analysed in the oral mucosa of unirradiated controls and during two weeks of fractionated irradiation.ResultsAdherens as well as tight junction marker proteins were rapidly and consistently upregulated in both the germinal as well as the functional layer of the oral mucosa. This represents a previously unknown parameter of the epithelial radiation response to clinically relevant fractionation protocols.ConclusionFractionated irradiation significantly enhanced the expression of all proteins investigated. This study revealed a new parameter of the epithelial radiation response to fractionated irradiation.Electronic supplementary materialThe online version of this article (10.1007/s00066-018-1302-6) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 93%

Upregulated epithelial junction expression represents a novel parameter of the epithelial radiation response to fractionated irradiation in oral mucosa

et al. 2018

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“…In contrast to p120-catenin, β-catenin was diffusely detected at the cytoplasm of basal cells in a high frequency. Stratified squamous epithelial stem cells reside at the basal cell layer [46]. Since WNT signaling is indispensable for the development and maintenance of epithelial stem cells [47], the cytoplasmic localization of β-catenin and the membrane-restricted weak expression of p120-catenin at the basal cells strengthen the understanding that catenins play a distinct role in oral epithelium physiology.…”

Section: Discussionmentioning

confidence: 99%

Concomitant Loss of p120-Catenin and β-Catenin Membrane Expression and Oral Carcinoma Progression with E-Cadherin Reduction

et al. 2013

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The binding of p120-catenin and β-catenin to the cytoplasmic domain of E-cadherin establishes epithelial cell-cell adhesion. Reduction and loss of catenin expression degrades E-cadherin-mediated carcinoma cell-cell adhesion and causes carcinomas to progress into aggressive states. Since both catenins are differentially regulated and play distinct roles when they dissociate from E-cadherin, evaluation of their expression, subcellular localization and the correlation with E-cadherin expression are important subjects. However, the same analyses are not readily performed on squamous cell carcinomas in which E-cadherin expression determines the disease progression. In the present study, we examined expression and subcellular localization of p120-catenin and β-catenin in oral carcinomas (n = 67) and its implications in the carcinoma progression and E-cadherin expression using immunohitochemistry. At the invasive front, catenin-membrane-positive carcinoma cells were decreased in the dedifferentiated (p120-catenin, P < 0.05; β-catenin, P < 0.05) and invasive carcinomas (p120-catenin, P < 0.01; β-catenin, P < 0.05) and with the E-cadherin staining (p120-catenin, P < 0.01; β-catenin, P < 0.01). Carcinoma cells with β-catenin cytoplasmic and/or nuclear staining were increased at the invasive front compared to the center of tumors (P < 0.01). Although the p120-catenin isoform shift from three to one associates with carcinoma progression, it was not observed after TGF-β, EGF or TNF-α treatments. The total amount of p120-catenin expression was decreased upon co-treatment of TGF-β with EGF or TNF-α. The above data indicate that catenin membrane staining is a primary determinant for E-cadherin-mediated cell-cell adhesion and progression of oral carcinomas. Furthermore, it suggests that loss of p120-catenin expression and cytoplasmic localization of β-catenin fine-tune the carcinoma progression.

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“…Elevated expression and greater nuclear localization of CTNNB1 have been reported for oral cancer and a multitude of other cancer types [56, 65]. While recent work has shown CTNNB1 immunostaining levels to be significantly associated with lymph node status, survival outcomes, and different invasive stages for oral cancers, data regarding the association of CTNNB1 methylation status for this disease have not [66].…”

Section: Genes Evincing Methylation Changes In Oral Squamous Cell mentioning

confidence: 99%

Methylation-Mediated Molecular Dysregulation in Clinical Oral Malignancy

Towle

Garnis

2012

Journal of Oncology

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Herein we provide a concise review of the state of methylation research as it pertains to clinical oral cancerous and precancerous tissues. We provide context for ongoing research efforts in this field and describe technologies that are presently being applied to analyze clinical specimens. We also discuss the various recurrent methylation changes that have been reported for oral malignancy (including those genes frequently silenced by promoter methylation and the small RNAs with activity modulated by methylation changes) and describe surrogate disease markers identified via epigenetic analysis of saliva and blood specimens from patients with oral cancer.

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Dickkopf (Dkk)-3 and β-catenin expressions increased in the transition from normal oral mucosal to oral squamous cell carcinoma

Cited by 34 publications

References 18 publications

Upregulated epithelial junction expression represents a novel parameter of the epithelial radiation response to fractionated irradiation in oral mucosa

Upregulated epithelial junction expression represents a novel parameter of the epithelial radiation response to fractionated irradiation in oral mucosa

Concomitant Loss of p120-Catenin and β-Catenin Membrane Expression and Oral Carcinoma Progression with E-Cadherin Reduction

Methylation-Mediated Molecular Dysregulation in Clinical Oral Malignancy

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