Epigenetic control of E-cadherin (CDH1) by CpG methylation in metastasising laryngeal cancer

Azarschab, Pia; Stembalska, Agnieszka; Lončar, Mirela Baus; Pfister, Markus; Sąsiadek, Maria M.; Blin, Nikolaus

doi:10.3892/or.10.2.501

Cited by 17 publications

(18 citation statements)

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“…Loss of expression of CDH13 has been found in parallel with the hypermethylated promoter CpG islands in various cancers (40). However, only one study of gliomas, in which investigation of CDH13 in low grade astrocytomas revealed no methylation patterns, had findings in accordance with our observations (18).…”

Section: G M T a N D R A R β M E T H Y L A T I O N I N H U M A N A supporting

confidence: 81%

High Incidence of MGMT and RARβ Promoter Methylation in Primary Glioblastomas: Association with Histopathological Characteristics, Inflammatory Mediators and Clinical Outcome

Piperi

Themistocleous

Papavassiliou³

et al. 2009

Mol Med

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Glioblastomas, the most frequent primary brain tumors in adults, are characterized by a highly aggressive, inflammatory and angiogenic phenotype. Methylation of CpG islands in cancer-related genes may serve as an epigenetic biomarker for glioblastoma diagnosis and prognosis. The aim of this study was to analyze the methylation status of four critical tumor-associated genes (MGMT, RARβ, RASSF1A, CDH13), and investigate possible links with inflammatory (interleukin [IL]-6, IL-8) and angiogenic mediators (vascular endothelial growth factor [VEGF], cyclooxygenase [COX]-2) and clinical outcome in 23 glioma samples (6 grade II astrocytomas, 17 grade IV glioblastomas). RARβ and MGMT genes were more frequently methylated in 70.58% and 58.8% of glioblastomas, respectively. RASSF1A and CDH13 displayed a similar methylation frequency (23.52%) in glioblastomas. No gene methylation was observed in grade II astrocytomas. Tumor grade correlated positively with MGMT and RARβ methylation (P = 0.005 and P = 0.019, respectively) and the extent of necrosis (P = 0.001 and P = 0.003). Interestingly, the marker of chronic inflammation, IL-6, was positively associated with methylation of MGMT (P = 0.004), RARβ (P = 0.002), and RASSF1A (P = 0.0081) as well as the total number of methylated genes (P < 0.0001), indicating the important role of IL-6 in maintaining promoter methylation of these genes. VEGF expression correlated positively with MGMT and RARβ methylation although these relationships were of marginal significance (P = 0.0679 and P = 0.0757). Kaplan-Meier univariate survival analysis indicated an unfavorable survival period in patients with MGMT methylation compared with those without methylation (P = 0.0474). Our study highlights the implication of MGMT and RARβ methylation in the aggressive phenotype of primary glioblastomas. The association of MGMT methylation with clinical outcome indicates its potential prognostic value.

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Section: G M T a N D R A R β M E T H Y L A T I O N I N H U M A N A supporting

confidence: 81%

High Incidence of MGMT and RARβ Promoter Methylation in Primary Glioblastomas: Association with Histopathological Characteristics, Inflammatory Mediators and Clinical Outcome

Piperi

Themistocleous

Papavassiliou³

et al. 2009

Mol Med

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“…Aberrant methylation of 5′CpG islands in the promoter region of CDH1 was reported for different types of mammary carcinomas and increased with malignant progression [95,96]. Other reports showed methylation in thyroid, hepatocellular, and prostate cancer, as well as in laryngeal cancer and colorectal cancer [97,98].…”

Section: Genetic and Epigenetic Inactivation Of E-cadherinmentioning

confidence: 98%

E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer

Schmalhofer

Brabletz

2009

Cancer Metastasis Rev

697

595

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The embryonic program 'epithelial-mesenchymal transition' (EMT) is activated during tumor invasion in disseminating cancer cells. Characteristic to these cells is a loss of E-cadherin expression, which can be mediated by EMT-inducing transcriptional repressors, e.g. ZEB1. Consequences of a loss of E-cadherin are an impairment of cell-cell adhesion, which allows detachment of cells, and nuclear localization of beta-catenin. In addition to an accumulation of cancer stem cells, nuclear beta-catenin induces a gene expression pattern favoring tumor invasion, and mounting evidence indicates multiple reciprocal interactions of E-cadherin and beta-catenin with EMT-inducing transcriptional repressors to stabilize an invasive mesenchymal phenotype of epithelial tumor cells.

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“…Furthermore, Ostler and colleagues stably transfected this truncated protein, DNMT3B7, into 293 cells (human embryonic kidney cells) and observed changes in methylation patterns of CpG islands that paralleled expression patterns noted in cancer cell lines [14] . One gene specifically noted in this paper was E-cadherin (CDH1), hypermethylation of which is correlated to a more aggressive cancer phenotype [15,16,17] . Ostler and colleagues demonstrated that hypermethylation of the E-cadherin CpG island paralleled a 2.19-fold decrease in gene expression [14] .…”

Section: Dnmt3b7 An Aberrant Dnmt3b Transcript Is Found In Virtuallmentioning

confidence: 99%

“…More specifically, hypermethylation and downregulation of E-cadherin was observed in the transfected cell lines. Loss of E-cadherin expression is a well-known marker of tumor progression [15,16,17] . β-catenin, a binding partner of E-cadherin, also displayed altered localization in transfected cells from the membrane to the nucleus.…”

Section: Dnmt3b7 Promotes Tumor Progression In Breast Cancer Cellsmentioning

confidence: 99%

The role of aberrant DNMT3Bs in tumor progression – a review

Hameed

Raimondi

2015

Can Cell Microenviron

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Epigenetic control of E-cadherin (CDH1) by CpG methylation in metastasising laryngeal cancer

Cited by 17 publications

References 0 publications

High Incidence of MGMT and RARβ Promoter Methylation in Primary Glioblastomas: Association with Histopathological Characteristics, Inflammatory Mediators and Clinical Outcome

High Incidence of MGMT and RARβ Promoter Methylation in Primary Glioblastomas: Association with Histopathological Characteristics, Inflammatory Mediators and Clinical Outcome

E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer

The role of aberrant DNMT3Bs in tumor progression – a review

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