We are analyzing https://link.springer.com/article/10.1007/s12272-018-01108-7.

Title:
Therapeutic implications of cancer epithelial-mesenchymal transition (EMT) | Archives of Pharmacal Research
Description:
The epithelial-mesenchymal transition (EMT) comprises an essential biological process involving cancer progression as well as initiation. While the EMT has been regarded as a phenotypic conversion from epithelial to mesenchymal cells, recent evidence indicates that it plays a critical role in stemness, metabolic reprogramming, immune evasion and therapeutic resistance of cancer cells. Interestingly, several transcriptional repressors including Snail (SNAI1), Slug (SNAI2) and the ZEB family constitute key players for EMT in cancer as well as in the developmental process. Note that the dynamic conversion between EMT and epithelial reversion (mesenchymal-epithelial transition, MET) occurs through variable intermediate-hybrid states rather than being a binary process. Given the close connection between oncogenic signaling and EMT repressors, the EMT has emerged as a therapeutic target or goal (in terms of MET reversion) in cancer therapy. Here we review the critical role of EMT in therapeutic resistance and the importance of EMT as a therapeutic target for human cancer.
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Keywords {🔍}

pubmed, cancer, article, google, scholar, cas, emt, cell, snail, transition, central, epithelialmesenchymal, kim, cells, signaling, tumor, phase, epithelial, therapeutic, development, kinase, tgfβ, zeb, clinical, expression, ecadherin, growth, biol, factor, receptor, res, patients, drug, study, progression, mesenchymal, breast, inhibitor, oncol, clin, pathway, lung, metastatic, advanced, lee, nat, resistance, slug, family, human,

Topics {✒️}

zinc-finger e-box binding tgf-beta-induced epithelial-mesenchymal transition blocks tgf-beta1-mediated epithelial mapk/erk-mediated zeb1 activity activate ras/raf/mek/erk tgf-β-mediated emt promotes multi-protein/transcriptional signaling pathways β-catenin/t-cell factor zinc-finger protein slug nf-κb signaling cascades article download pdf transforming growth factor-beta hypoxia-inducible factor 1α tgf-beta-induced epithelial emt-tfs emt-transcriptional factors growth factor-i-dependent links epithelial-mesenchymal transition axin2-mediated nuclear export emt-activating transcriptional factors translational/post-translational regulations mapk/egr-1-mediated upregulation e-cadherin repressor snail tgf-beta-induced activation wnt/beta-catenin signaling tgf-beta1-induced emt wnt/beta-catenin pathway epithelial-mesenchymal cell transition cancer epithelial-mesenchymal transition variable intermediate-hybrid states snail-expressing mdck cells wnt/β-catenin pathway regulate epithelial-mesenchymal transitions tgf-β signaling pathway tgf-β blocking antibody emt-activating transcription factors pre-planned interim analysis gsk-3-dependent phosphorylation motif targets tgf-β proteins increased transcriptional activity decreased e-cadherin expression promote emt-transcriptional factors double-negative feedback loop de jesus-acosta small-molecule alk5 inhibitors wnt/β-catenin/snail small-cell lung cancer disrupting axin-gsk3 interaction tgf-beta receptor function enhance tgf-β1 expression repressing e-cadherin expression

Questions {❓}

Yochum GS (2012) AXIN2: tumor suppressor, oncogene or both in colorectal cancer?

Schema {🗺️}

WebPage:
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         headline:Therapeutic implications of cancer epithelial-mesenchymal transition (EMT)
         description:The epithelial-mesenchymal transition (EMT) comprises an essential biological process involving cancer progression as well as initiation. While the EMT has been regarded as a phenotypic conversion from epithelial to mesenchymal cells, recent evidence indicates that it plays a critical role in stemness, metabolic reprogramming, immune evasion and therapeutic resistance of cancer cells. Interestingly, several transcriptional repressors including Snail (SNAI1), Slug (SNAI2) and the ZEB family constitute key players for EMT in cancer as well as in the developmental process. Note that the dynamic conversion between EMT and epithelial reversion (mesenchymal-epithelial transition, MET) occurs through variable intermediate-hybrid states rather than being a binary process. Given the close connection between oncogenic signaling and EMT repressors, the EMT has emerged as a therapeutic target or goal (in terms of MET reversion) in cancer therapy. Here we review the critical role of EMT in therapeutic resistance and the importance of EMT as a therapeutic target for human cancer.
         datePublished:2019-01-16T00:00:00Z
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      headline:Therapeutic implications of cancer epithelial-mesenchymal transition (EMT)
      description:The epithelial-mesenchymal transition (EMT) comprises an essential biological process involving cancer progression as well as initiation. While the EMT has been regarded as a phenotypic conversion from epithelial to mesenchymal cells, recent evidence indicates that it plays a critical role in stemness, metabolic reprogramming, immune evasion and therapeutic resistance of cancer cells. Interestingly, several transcriptional repressors including Snail (SNAI1), Slug (SNAI2) and the ZEB family constitute key players for EMT in cancer as well as in the developmental process. Note that the dynamic conversion between EMT and epithelial reversion (mesenchymal-epithelial transition, MET) occurs through variable intermediate-hybrid states rather than being a binary process. Given the close connection between oncogenic signaling and EMT repressors, the EMT has emerged as a therapeutic target or goal (in terms of MET reversion) in cancer therapy. Here we review the critical role of EMT in therapeutic resistance and the importance of EMT as a therapeutic target for human cancer.
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         EMT
         Therapeutic resistance
         Oncogenes
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               type:PostalAddress
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            address:
               name:Department of Oral Pathology, Oral Cancer Research Institute, Yonsei University College of Dentistry, Seoul, Republic of Korea
               type:PostalAddress
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      email:[email protected]
      name:Jong In Yook
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      affiliation:
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            address:
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      name:Department of Oral Pathology, Oral Cancer Research Institute, Yonsei University College of Dentistry, Seoul, Republic of Korea
      name:Department of Oral Pathology, Oral Cancer Research Institute, Yonsei University College of Dentistry, Seoul, Republic of Korea

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