We are analyzing https://link.springer.com/article/10.1186/s12943-016-0502-x.

Title:
Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications | Molecular Cancer
Description:
The epithelial to mesenchymal transition (EMT) is a biological process in which a non-motile epithelial cell changes to a mesenchymal phenotype with invasive capacities. This phenomenon has been well documented in multiple biological processes including embryogenesis, fibrosis, tumor progression and metastasis. The hallmark of EMT is the loss of epithelial surface markers, most notably E-cadherin, and the acquisition of mesenchymal markers including vimentin and N-cadherin. The downregulation of E-cadherin during EMT can be mediated by its transcriptional repression through the binding of EMT transcription factors (EMT-TFs) such as SNAIL, SLUG and TWIST to E-boxes present in the E-cadherin promoter. Additionally, EMT-TFs can also cooperate with several enzymes to repress the expression of E-cadherin and regulate EMT at the epigenetic and post- translational level. In this review, we will focus on epigenetic and post- translational modifications that are important in EMT. In addition, we will provide an overview of the various therapeutic approaches currently being investigated to undermine EMT and hence, the metastatic progression of cancer as well.
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Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, emt, cell, expression, central, ecadherin, snail, cells, histone, transition, epithelial, protein, transcription, methylation, cdh, tumor, metastasis, breast, promoter, epithelialmesenchymal, epigenetic, mesenchymal, twist, genes, phosphorylation, results, regulation, modifications, proteins, dna, hdac, modification, gene, sumoylation, activation, target, biol, progression, sirt, transcriptional, zeb, human, development, hifα, important,

Topics {✒️}

tgfbeta-induced epithelial-mesenchymal transition hypoxia-induced epithelial-mesenchymal transition corepressor c-terminal-binding protein o-linked β-n-acetylglucosamine article serrano-gomez article download pdf uridine 5′-diphospho-n-acetylglucosamine e-cadherin invasion-suppressor gene α-ketoglutarate dependent demethylase snail-mediated e-cadherin repression e-cadherin-integrin crosstalk twist/mi2/nurd protein complex zeb/mir-200 feedback loop zeb/mir-200 feedback loop tgf-β activates kdm6b post-translational modifications represents o-linked n-acetylglucosaminylation mi 2/nurd/mta2 complex e3-ubiquitin ligase smurf-1 sentrin/sumo-specific proteases pdhs hydroxylate hif-1α zeb1 represses e-cadherin dna-binding domain called e-cadherin germline mutations tβri- tβrii hetero-dimerize hypoxia inducible factor-1 spindle-shaped cell morphology epithelial-mesenchymal transition process ferrell jr je genome-scale epigenetic reprogramming cell-cell contact proteins dna methylation-independent context e-cadherin gene expression de andrade jp process include n-cadherin regulates hif-1α degradation pkd1-fbxo11-snail axis smad-interacting protein 1 normal adult cells/tissues explore potential applications gsk-3beta-mediated phosphorylation oxygen-dependent degradation domain bhlh factor e2 post-translational modification characterized specific cell-surface proteins multi-protein complexes composed prevent e-cadherin expression privacy choices/manage cookies snai1-mediated transcriptional repression tyrosine kinase receptors

Questions {❓}

The ZEB/miR-200 feedback loop--a motor of cellular plasticity in development and cancer?
The relevance of EMT in breast cancer metastasis: Correlation or causality?

Schema {🗺️}

WebPage:
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         headline:Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications
         description:The epithelial to mesenchymal transition (EMT) is a biological process in which a non-motile epithelial cell changes to a mesenchymal phenotype with invasive capacities. This phenomenon has been well documented in multiple biological processes including embryogenesis, fibrosis, tumor progression and metastasis. The hallmark of EMT is the loss of epithelial surface markers, most notably E-cadherin, and the acquisition of mesenchymal markers including vimentin and N-cadherin. The downregulation of E-cadherin during EMT can be mediated by its transcriptional repression through the binding of EMT transcription factors (EMT-TFs) such as SNAIL, SLUG and TWIST to E-boxes present in the E-cadherin promoter. Additionally, EMT-TFs can also cooperate with several enzymes to repress the expression of E-cadherin and regulate EMT at the epigenetic and post- translational level. In this review, we will focus on epigenetic and post- translational modifications that are important in EMT. In addition, we will provide an overview of the various therapeutic approaches currently being investigated to undermine EMT and hence, the metastatic progression of cancer as well.
         datePublished:2016-02-24T00:00:00Z
         dateModified:2016-02-24T00:00:00Z
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            Therapy
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      headline:Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications
      description:The epithelial to mesenchymal transition (EMT) is a biological process in which a non-motile epithelial cell changes to a mesenchymal phenotype with invasive capacities. This phenomenon has been well documented in multiple biological processes including embryogenesis, fibrosis, tumor progression and metastasis. The hallmark of EMT is the loss of epithelial surface markers, most notably E-cadherin, and the acquisition of mesenchymal markers including vimentin and N-cadherin. The downregulation of E-cadherin during EMT can be mediated by its transcriptional repression through the binding of EMT transcription factors (EMT-TFs) such as SNAIL, SLUG and TWIST to E-boxes present in the E-cadherin promoter. Additionally, EMT-TFs can also cooperate with several enzymes to repress the expression of E-cadherin and regulate EMT at the epigenetic and post- translational level. In this review, we will focus on epigenetic and post- translational modifications that are important in EMT. In addition, we will provide an overview of the various therapeutic approaches currently being investigated to undermine EMT and hence, the metastatic progression of cancer as well.
      datePublished:2016-02-24T00:00:00Z
      dateModified:2016-02-24T00:00:00Z
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      pageEnd:14
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12943-016-0502-x
      keywords:
         Cancer
         Metastasis
         Epigenetic
         Methylation
         Therapy
         Cancer Research
         Oncology
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                     type:PostalAddress
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                     name:Pontificia Universidad Javeriana, Bogota, Colombia
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         name:Pontificia Universidad Javeriana, Bogota, Colombia
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            address:
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               type:PostalAddress
            type:Organization
            name:Pontificia Universidad Javeriana
            address:
               name:Pontificia Universidad Javeriana, Bogota, Colombia
               type:PostalAddress
            type:Organization
      name:Mazvita Maziveyi
      affiliation:
            name:LSUHSC School of Medicine
            address:
               name:Department of Biochemistry and Molecular Biology, LSUHSC School of Medicine, New Orleans, USA
               type:PostalAddress
            type:Organization
      name:Suresh K. Alahari
      affiliation:
            name:LSUHSC School of Medicine
            address:
               name:Department of Biochemistry and Molecular Biology, LSUHSC School of Medicine, New Orleans, USA
               type:PostalAddress
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PostalAddress:
      name:Department of Biochemistry and Molecular Biology, LSUHSC School of Medicine, New Orleans, USA
      name:Pontificia Universidad Javeriana, Bogota, Colombia
      name:Department of Biochemistry and Molecular Biology, LSUHSC School of Medicine, New Orleans, USA
      name:Department of Biochemistry and Molecular Biology, LSUHSC School of Medicine, New Orleans, USA

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