E‐cadherin regulators are differentially expressed in the epithelium and stroma of keratocystic odontogenic tumors

Porto, Lia Pontes Arruda; Santos, Jean Nunes dos; Ramalho, Luciana Maria Pedreira; Figueiredo, Andreia Cristina Leal; Júnior, Bráulio Carneiro; Gurgel, Clarissa Araújo Silva; Paiva, Katiúcia Batista Silva; Xavier, Flávia Caló Aquino

doi:10.1111/jop.12382

Cited by 12 publications

(10 citation statements)

References 41 publications

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“…When the left and right palatine processes fuse after contact, epithelial cells lose their polarity in the epithelial cord and either reconstruct their cytoskeleton to convert to mesenchymal cell traits, which is called the epithelial-mesenchymal transition (EMT), or undergo apoptosis [35][36][37][38][39][40]. In this study, E-cadherin-, β-catenin-, and α-catenin-positive cells were found in the midline epithelial cord of the anterior palate in the TCDD-treated group, and TUNEL-positive cells were found in the same area.…”

Section: Discussionmentioning

confidence: 99%

Histological and Immunohistochemical Studies to Determine the Mechanism of Cleft Palate Induction after Palatal Fusion in Mice Exposed to TCDD

Sakuma

Imura

Yamada

et al. 2022

IJMS

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Rupture of the basement membrane in fused palate tissue can cause the palate to separate after fusion in mice, leading to the development of cleft palate. Here, we further elucidate the mechanism of palatal separation after palatal fusion in 8–10-week-old ICR female mice. On day 12 of gestation, 40 μg/kg of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), sufficient to cause cleft palate in 100% of mice, was dissolved in 0.4 mL of olive oil containing toluene and administered as a single dose via a gastric tube. Fetal palatine frontal sections were observed by H&E staining, and epithelial cell adhesion factors, apoptosis, and cell proliferation were observed from the anterior to posterior palate. TUNEL-positive cells and Ki67-positive cells were observed around the posterior palatal dissection area of the TCDD-treated group. Moreover, in fetal mice exposed to TCDD, some fetuses exhibited cleft palate dehiscence during fusion. The results suggest that palatal dehiscence may be caused by abnormal cell proliferation in epithelial tissues, decreased intercellular adhesion, and inhibition of mesenchymal cell proliferation. By elucidating the mechanism of cleavage after palatal fusion, this research can contribute to establishing methods for the prevention of cleft palate development.

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Section: Discussionmentioning

confidence: 99%

Histological and Immunohistochemical Studies to Determine the Mechanism of Cleft Palate Induction after Palatal Fusion in Mice Exposed to TCDD

Sakuma

Imura

Yamada

et al. 2022

IJMS

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“…Various EMT induced factors like inflammatory factors may change the balance between epithelial character maintenance and EMT. The disruption of this function may be involved in root morphology abnormalities and the development of odontogenic cysts and tumors originating from HERS and ERM 24 . In future, exhaustive single cell analysis about signaling associated with EMT is needed.…”

Section: Discussionmentioning

confidence: 99%

Semaphorin‐RhoA signaling regulates HERS maintenance by acting against TGF‐β‐induced EMT

Azumane

Ikezaki

Otsu

et al. 2022

J of Periodontal Research

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Background and Objectives Hertwig's epithelial root sheath (HERS) plays a role in root dentin formation. It produces the epithelial rests of Malassez (ERM) for the induction of periodontal tissue development during root formation. Although ERM is thought to be caused by epithelial–mesenchymal transition (EMT), the mechanism by which HERS is maintained as epithelium is unknown. Here, we aimed to elucidate the molecular mechanisms regulating the relationship between HERS maintenance and ERM development. Methods To understand the relationship between HERS and ERM development during root formation, we observed the developing molar root using cytokeratin14 (CK14) Cre/tdTomato mice via stereomicroscopy. The relationship between semaphorin and transforming growth factor (TGF) signaling in the maintenance of HERS and ERM development was examined using CK14cre/R26‐tdTomato mice and a HERS cell line. Results tdTomato‐positive cells were observed on HERS and the migrating cells from HERS. The migrating cells showed reduced E‐cadherin expression. In contrast, HERS cells expressed semaphorin receptors and active RhoA. Semaphorin signaling was associated with RhoA activation and cell–cell adhesion, while TGF‐β induced decreased E‐cadherin and active RhoA expression, and consequently enhanced cell migration. Conclusion HERS induces root formation by controlling epithelial maintenance and EMT through the opposing effects of semaphorin and TGF‐β signaling.

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“…In this way, the cell increases its ability to invade, migrate, and generate metastasis. The dissociation of tumor cells across tissues due to changes in cell-cell adhesion is one of the main causes of the tumor's invasive capacity [8], being a possible explanation for the aggressive behavior of OK.…”

Section: Introductionmentioning

confidence: 99%

“…The concept of EMT in tumor metastasis formation is based on observations that epithelial carcinoma cells that acquired mesenchymal markers such as vimentin and loss of cell-cell adhesion molecules such as E-cadherin [9] were associated with a higher metastatic potential. Currently, the most commonly used markers for EMT verification are vimentin, fibronectin and N-cadherin (mesenchymal markers), E-cadherin (epithelial markers) and Snail and Slug (transcription factors) [8,9].…”

Section: Introductionmentioning

confidence: 99%

“…Evidence for the involvement of EMT in OK progression is still limited [8], however, dysregulation of these proteins may explain the molecular mechanism by which these lesions develop. E-cadherin is the protein member which connects epithelial cells together at adherens junctions and it plays an important role in epithelial cell adhesion and the loss of its function is a major contributor to cancer progression because the majority of solid tumors are carcinomas that arise from epithelial tissue [10].…”

Section: Introductionmentioning

confidence: 99%

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Epithelial-mesenchymal markers and their correlation with clinical aspects in odontogenic keratocysts

Vendruscolo

Lessa

Ioshii

et al. 2022

RGO, Rev. Gaúch. Odontol.

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Objective: Odontogenic keratocysts have a high recurrence rate and aggressive clinical behavior. The event called epithelial-mesenchymal transition is a process in which the epithelial cell loses its epithelial characteristics and acquires properties typical of mesenchymal cells. Studies have already demonstrated that odontogenic keratocysts has expression of tumor markers, but the lack of clarification about its development mechanism and molecular composition makes the therapeutic options remain limited. The aim of this study is to evaluate the expression of epithelial-mesenchymal transition marker proteins in these lesions, correlating the expression of these proteins with clinical aspects of each case. Methods: Patients with odontogenic keratocysts diagnoses, treated by the Department of Oral and Maxillofacial Surgery of the Erasto Gaertner Hospital, Curitiba, Brazil in the period between 2016 and 2019 were evaluated by immunohistochemical analysis, to assess the expression of epithelial-mesenchymal transition markers (Vimentin, beta-catenin and E-cadherin) by qualitative analysis. Results: Eighteen patients were included, with a mean age of 43 years, and most of them were male. The mandible was more affected than the maxilla. No association between the clinical characteristics of the cysts and the immunohistochemical profile for epithelial-mesenchymal transition proteins was observed. Conclusion: The positivity of E-cadherin and negativity of vimentin demonstrates that its function is preserved. Loss of function of E-cadherin is associated with worse prognosis. The identification of the epithelial-mesenchymal transition process as a prognostic marker for odontogenic cysts and tumors could be an important tool for defining treatment.

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E‐cadherin regulators are differentially expressed in the epithelium and stroma of keratocystic odontogenic tumors

Cited by 12 publications

References 41 publications

Histological and Immunohistochemical Studies to Determine the Mechanism of Cleft Palate Induction after Palatal Fusion in Mice Exposed to TCDD

Histological and Immunohistochemical Studies to Determine the Mechanism of Cleft Palate Induction after Palatal Fusion in Mice Exposed to TCDD

Semaphorin‐RhoA signaling regulates HERS maintenance by acting against TGF‐β‐induced EMT

Epithelial-mesenchymal markers and their correlation with clinical aspects in odontogenic keratocysts

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