BVES regulates EMT in human corneal and colon cancer cells and is silenced via promoter methylation in human colorectal carcinoma

Williams, Christopher S.; Zhang, Baolin; Smith, J. Joshua; Jayagopal, Ashwath; Barrett, Caitlyn W.; Pino, Christopher J.; Russ, Patricia K.; Presley, S.–H.; Peng, Dun Fa; Rosenblatt, Daniel O.; Haselton, Frederick R.; Yang, Jin; Washington, Mary Kay; Chen, Xi; Eschrich, Steven; Yeatman, Timothy J.; El-Rifai, Wael; Beauchamp, R. Daniel; Chang, Min S.

doi:10.1172/jci44228

Cited by 61 publications

(107 citation statements)

References 53 publications

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“…A report, published while this manuscript was in preparation, demonstrated that claudin-5 is decreased in bleomycininduced pulmonary fibrosis (39), which indicated that decreased CLDN5 expression may be involved in epithelial-mesenchymal transition (EMT). EMT often involves promoter methylation to turn off epithelial genes (40,41). The hypermethylation of claudin-5 in IPF lung tissues could be an indicator of EMT occurring in specific cell populations.…”

Section: Discussionmentioning

confidence: 99%

Altered DNA Methylation Profile in Idiopathic Pulmonary Fibrosis

Sanders

Ambalavanan²,

Halloran³

et al. 2012

Am J Respir Crit Care Med

200

136

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Rationale: DNA methylation is an important epigenetic mechanism, which often occurs in response to environmental stimuli and is crucial in regulating gene expression. It is likely that epigenetic alterations contribute to pathogenesis in idiopathic pulmonary fibrosis (IPF). Objectives: To determine the DNA methylation changes in IPF and their effects on gene expression. Methods: Total DNA methylation and DNA methyltransferase expression were compared in IPF and normal control lung tissues. IPF and normal tissues were subjected to comparative analysis of genomewide DNA methylation and RNA expression using DNA hybridization to the Illumina HumanMethylation27 BeadChip and RNA hybridization to Illumina HumanHT-12 BeadChip. Functional analyses of differentially expressed and differentially methylated genes were done. Selected genes were validated at DNA, RNA, and protein levels. Measurements and Main Results: DNA methylation status was altered in IPF. IPF samples demonstrated higher DNA methyltransferase expression without observed alterations in global DNA methylation. Genome-wide differences in DNA methylation status and RNA expression were demonstrated by array hybridization. Among the genes whose DNA methylation status and RNA expression were both significantly altered, 16 genes were hypermethylated in DNA associated with decreased mRNA expression or vice versa. We validated CLDN5, ZNF467, TP53INP1, and DDAH1 genes at the level of DNA methylation status, RNA, and protein-level expression. Conclusions: Changes in DNA methylation correspond to altered mRNA expression of a number of genes, some with known and others with previously uncharacterized roles in IPF, suggesting that DNA methylation is important in the pathogenesis of IPF.

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Section: Discussionmentioning

confidence: 99%

Altered DNA Methylation Profile in Idiopathic Pulmonary Fibrosis

Sanders

Ambalavanan²,

Halloran³

et al. 2012

Am J Respir Crit Care Med

200

136

View full text Add to dashboard Cite

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“…In mice treated with NS, Lipo, or Lipo ϩ NC shRNA, measurable endometrial fragments after a 25-day incubation were observed, with an average volume of 28.36, 18.17, and 19.74 mm 3 , respectively (Fig. 8, A and F).…”

Section: Anxa2 Knockdown Compromises Growth Metastasis and Proangiomentioning

confidence: 98%

“…Epithelial to mesenchymal transition (EMT) 1 is a process characterized by a loss of polarity of epithelial cells and transition to a mesenchymal phenotype (3). It has been reported both under physiological situations like wound healing (4) and during development as well as in malignant cells undergoing invasion and metastasis, which could be initiated through a variety of stimuli, including hormonal turbulence, genetic mutation, or hypoxia (5).…”

mentioning

confidence: 99%

Proteomics Identification of Annexin A2 as a Key Mediator in the Metastasis and Proangiogenesis of Endometrial Cells in Human Adenomyosis

Zhou

et al. 2012

Molecular & Cellular Proteomics

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Adenomyosis is a common estrogen-dependent disorder of females characterized by a downward extension of the endometrium into the uterine myometrium and neovascularization in ectopic lesions. It accounts for chronic pelvic pain, dysmenorrhea, menorrhagia, and infertility in 8.8 -61.5% women worldwide. However, the molecular mechanisms for adenomyosis development remain poorly elucidated. Here, we utilized a two-dimensional polyacrylamide gel electrophoresis/MS-based proteomics analysis to compare and identify differentially expressed proteins in matched ectopic and eutopic endometrium of adenomyosis patients. A total of 93 significantly altered proteins were identified by tandem MS analysis. Further cluster analysis revealed a group of estrogen-responsive proteins as dysregulated in adenomyosis, among which annexin A2, a member of annexin family proteins, was found up-regulated most significantly in the ectopic endometrium of adenomyosis compared with its eutopic counterpart. Overexpression of ANXA2 was validated in ectopic lesions of human adenomyosis and was found to be tightly correlated with markers of epithelial to mesenchymal transition and dysmenorrhea severity of adenomyosis patients. Functional analysis demonstrated that estrogen could remarkably up-regulate ANXA2 and induce epithelial to mesenchymal transition in an in vitro adenomyosis model. Enforced expression of ANXA2 could mediate phenotypic mesenchymal-like cellular changes, with structural and functional alterations in a ␤-catenin/T-cell factor (Tcf) signaling-associated manner, which could be reversed by inhibition of ANXA2 expression. We also proved that enforced expression of ANXA2 enhanced the proangiogenic capacity of adenomyotic endometrial cells through HIF-1␣/VEGF-A pathway. In vivo, we demonstrated that ANXA2 inhibition abrogated endometrial tissue growth, metastasis, and angiogenesis in an adenomyosis nude mice model and significantly alleviated hyperalgesia. Taken together, our data unraveled a dual role for ANXA2 in the pathogenesis of human adenomyosis through conferring endometrial cells both metastatic potential and proangiogenic capacity, which could serve as a potential therapeutic target for the treatment of adenomyosis patients.

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“…BVES is another transmembrane component of tight junctions that is downregulated during the epithelial-to-mesenchymal transition (EMT) (Han et al, 2014;Williams et al, 2011). Reexpression of BVES in colorectal cancer cells is sufficient to repress proliferation and metastasis, indicating that it also has tumour suppressive activities.…”

Section: Regulation Of Cell Behaviour and Survival By Transmembrane Pmentioning

confidence: 99%

Signalling at tight junctions during epithelial differentiation and microbial pathogenesis

Zihni

Balda

Matter

2014

Journal of Cell Science

106

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Tight junctions are a component of the epithelial junctional complex, and they form the paracellular diffusion barrier that enables epithelial cells to create cellular sheets that separate compartments with different compositions. The assembly and function of tight junctions are intimately linked to the actomyosin cytoskeleton and, hence, are under the control of signalling mechanisms that regulate cytoskeletal dynamics. Tight junctions not only receive signals that guide their assembly and function, but transmit information to the cell interior to regulate cell proliferation, migration and survival. As a crucial component of the epithelial barrier, they are often targeted by pathogenic viruses and bacteria, aiding infection and the development of disease. In this Commentary, we review recent progress in the understanding of the molecular signalling mechanisms that drive junction assembly and function, and the signalling processes by which tight junctions regulate cell behaviour and survival. We also discuss the way in which junctional components are exploited by pathogenic viruses and bacteria, and how this might affect junctional signalling mechanisms.

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BVES regulates EMT in human corneal and colon cancer cells and is silenced via promoter methylation in human colorectal carcinoma

Cited by 61 publications

References 53 publications

Altered DNA Methylation Profile in Idiopathic Pulmonary Fibrosis

Altered DNA Methylation Profile in Idiopathic Pulmonary Fibrosis

Proteomics Identification of Annexin A2 as a Key Mediator in the Metastasis and Proangiogenesis of Endometrial Cells in Human Adenomyosis

Signalling at tight junctions during epithelial differentiation and microbial pathogenesis

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