CDH4 suppresses the progression of salivary adenoid cystic carcinoma via E-cadherin co-expression

Xie, Jian; Yan, Feng; Lin, Ting; Huang, Xiaoyu; Gan, Rui‐Huan; Zhao, Yong; Su, Bogong; Ding, Lin‐Can; Shen, Lin; Chen, Jiang; Lin, Lisong; Lin, Xu; Zheng, Dali; Lu, You‐Guang

doi:10.18632/oncotarget.12821

Cited by 17 publications

(16 citation statements)

References 35 publications

(34 reference statements)

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“…Similar to mucosal melanoma, the availability of reliable preclinical models is limited [ 51 ], and most published studies on expression and regulation of EMT-related proteins rely on retrospective studies with FFPE (Formalin-fixed paraffin-embedded) tissue samples. However, reduced expression of E-cadherin in salivary ACCs could be described as compared to paraneoplastic normal salivary tissue [ 52 ]. SNAI2 and E-cadherin expression were negatively associated in a cohort of 115 salivary ACC.…”

Section: Emt-like Phenotype In Salivary Gland Malignanciesmentioning

confidence: 99%

“…SNAI2 and E-cadherin expression were negatively associated in a cohort of 115 salivary ACC. High SNAI2 and low E-cadherin expression were significantly correlated with perineural invasion [ 52 ]. Yi et al investigated the expression of BMI1—a major component of the polycomb group complex 1 and a candidate stem cell marker—together with EMT-related proteins SNAI1, SNAI2, and E-cadherin in a cohort of 102 ACC patients [ 53 ].…”

Section: Emt-like Phenotype In Salivary Gland Malignanciesmentioning

confidence: 99%

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Epithelial-to-Mesenchymal Transition in the Pathogenesis and Therapy of Head and Neck Cancer

Thierauf

Veit

Heß

2017

Cancers

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Head and neck cancer (HNC) is one of the most prevalent human malignancies worldwide, with a high morbidity and mortality. Implementation of interdisciplinary treatment modalities has improved the quality of life, but only minor changes in overall survival have been achieved over the past decades. Main causes for treatment failure are an aggressive and invasive tumor growth in combination with a high degree of intrinsic or acquired treatment resistance. A subset of tumor cells gain these properties during malignant progression by reactivating a complex program of epithelia-to-mesenchymal transition (EMT), which is integral in embryonic development, wound healing, and stem cell behavior. EMT is mediated by a core set of key transcription factors, which are under the control of a large range of developmental signals and extracellular cues. Unraveling molecular principles that drive EMT provides new concepts to better understand tumor cell plasticity and response to established as well as new treatment modalities, and has the potential to identify new drug targets for a more effective, less toxic, and individualized therapy of HNC patients. Here, we review the most recent findings on the clinical relevance of a mesenchymal-like phenotype for HNC patients, including more rare cases of mucosal melanoma and adenoid cystic carcinoma.

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Section: Emt-like Phenotype In Salivary Gland Malignanciesmentioning

confidence: 99%

Section: Emt-like Phenotype In Salivary Gland Malignanciesmentioning

confidence: 99%

Epithelial-to-Mesenchymal Transition in the Pathogenesis and Therapy of Head and Neck Cancer

Thierauf

Veit

Heß

2017

Cancers

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“…Alaraudanjoki et al [34] Cadherin 4 (CDH4) rs2426986, rs16984837, and rs6101273 e encoded protein (R-cadherin) is a calcium-dependent cell-cell adhesion glycoprotein, which is highly expressed in oral mucosa and also linked to both Wnt and FGF signaling [39]. Recently, it has been shown that CDH4 also promotes the expression of E-cadherin [40], which plays a crucial role in enamel development [41].…”

Section: Ameloblastin (Ambn) Rs4694075mentioning

confidence: 99%

Genetic Aspects of Dental Erosive Wear and Dental Caries

Tulek

Mulic

Runningen

et al. 2021

International Journal of Dentistry

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Objectives. The present review aims to give an overview of the literature focusing on novel genetic aspects of dental erosion and dental caries. Once the tooth erupts into the oral cavity, the regenerative capability of enamel is fundamentally limited due to the loss of dental epithelium during eruption. The susceptibility or resistance to dental erosion and caries is presumably a result of environmental, phenotypic, and/or genetic influence. Even though it is evident that individuals frequently exposing their teeth to acid and sugar are at high risk of developing dental erosion and caries, the findings exclusively based on these factors are elusive. Data resources and study selection. The present review was based on data collected from the National Library of Medicine database with different combinations of the following terms: “tooth,” “dental,” “dentin,” “enamel,” “erosion,” “erosive wear,” “caries,” “decay,” “gene,” and “genetic.” A total of forty-six studies met the inclusion criteria. Data were extracted by one reviewer and verified by another. Conclusion. The high prevalence of erosion and caries among certain groups, and observations that not all individuals appearing to be at risk develop these lesions, has sparked research on identifying genetic effects to these conditions. A connection of genome-wide and candidate gene studies has increased considerably in the literature. This review reveals largely varying success among studies, demonstrating the difficulties of developing the study with adequate sample sizes and durable phenotype definitions that permit enough statistical power to identify genetic contributors.

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“…Moreover, Zhang et al (2000) noticed a correlation between E-cadherin expression and the degree of salivary ACC cell differentiation [28]. More recently, Xie et al (2016) recorded that cadherin 4 (CDH4) gene, responsible for retinal cadherin (R-cadherin) encoding, could inhibit the growth and metastasis of salivary ACC via co-expression with E-cadherin [29]. Zhao et al (2013) [30], similar to other authors [31,32], reported that reduced E-cadherin expression in salivary ACC correlated with solid type, advanced stages, perineural invasion, recurrences and distant metastasis.…”

Section: Figure 7 -(A) Statistical Analysis Proving a Strong Correlation Between E-cadherin And Vimentin Ihc Scores (R=0999 P=0027) (B) Amentioning

confidence: 99%

Immunophenotypical alterations with impact on the epithelial–mesenchymal transition (EMT) process in salivary gland adenoid cystic carcinomas

Belulescu

Mărgăritescu

Dumitrescu³

et al. 2020

Rom J Morphol Embryol

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Adenoid cystic carcinoma (ACC) is one of the most common malignant salivary glands neoplasms with an indolent clinical course, slow-growing but locally aggressive and quite often with delayed recurrence and distant metastasis. In order to elucidate this tumoral behavior, we conducted an immunohistochemical study investigating the alterations of epithelial phenotype with anti-cytokeratin (CK) AE1/AE3 and anti-E-cadherin antibodies, and the acquisition of mesenchymal phenotype with vimentin, fibronectin, N-cadherin and P-cadherin in salivary ACCs. Thus, we recorded a reduction of CK AE1/AE3, E-cadherin, P-cadherin and fibronectin reactivity in the solid variant and especially in the cells from the periphery of invasive neoplastic proliferations, regardless histological type. These phenotypical alterations suggest the involvement of the epithelial-mesenchymal transition (EMT) process in the progression of salivary ACCs.

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CDH4 suppresses the progression of salivary adenoid cystic carcinoma via E-cadherin co-expression

Cited by 17 publications

References 35 publications

Epithelial-to-Mesenchymal Transition in the Pathogenesis and Therapy of Head and Neck Cancer

Epithelial-to-Mesenchymal Transition in the Pathogenesis and Therapy of Head and Neck Cancer

Genetic Aspects of Dental Erosive Wear and Dental Caries

Immunophenotypical alterations with impact on the epithelial–mesenchymal transition (EMT) process in salivary gland adenoid cystic carcinomas

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