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Title:
EMT-activating transcription factors in cancer: beyond EMT and tumor invasiveness | Cellular and Molecular Life Sciences
Description:
Cancer is a complex multistep process involving genetic and epigenetic changes that eventually result in the activation of oncogenic pathways and/or inactivation of tumor suppressor signals. During cancer progression, cancer cells acquire a number of hallmarks that promote tumor growth and invasion. A crucial mechanism by which carcinoma cells enhance their invasive capacity is the dissolution of intercellular adhesions and the acquisition of a more motile mesenchymal phenotype as part of an epithelial-to-mesenchymal transition (EMT). Although many transcription factors can trigger it, the full molecular reprogramming occurring during an EMT is mainly orchestrated by three major groups of transcription factors: the ZEB, Snail and Twist families. Upregulated expression of these EMT-activating transcription factors (EMT-ATFs) promotes tumor invasiveness in cell lines and xenograft mice models and has been associated with poor clinical prognosis in human cancers. Evidence accumulated in the last few years indicates that EMT-ATFs also regulate an expanding set of cancer cell capabilities beyond tumor invasion. Thus, EMT-ATFs have been shown to cooperate in oncogenic transformation, regulate cancer cell stemness, override safeguard programs against cancer like apoptosis and senescence, determine resistance to chemotherapy and promote tumor angiogenesis. This article reviews the expanding portfolio of functions played by EMT-ATFs in cancer progression.
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Keywords {🔍}
google, scholar, article, pubmed, cas, cancer, cell, transition, snail, cells, expression, res, zeb, twist, biol, epithelialmesenchymal, wang, ecadherin, carcinoma, epithelial, transcription, tumor, mol, yang, breast, human, regulation, metastasis, sci, zhang, liu, oncogene, transcriptional, factors, emt, promotes, slug, mesenchymal, epithelialtomesenchymal, factor, protein, invasion, lee, progression, growth, clin, stem, chem, gene, van,
Topics {✒️}
β-catenin/tcf4 complex induces hypoxia-inducible factor-1-dependent repression growth factor-i-dependent transforming growth factor-β trkb-induced epithelial-mesenchymal transition trkb-induced epithelial-mesenchymal transition snail1-induced epithelial-mesenchymal transition twist1-induced epithelial-mesenchymal transition twist/mi2/nurd protein complex zinc finger/homeodomain repressor f-box protein ppa zinc finger/homeodomain repressors month download article/chapter cell-type-specific transcriptional regulator e-cadherin preserved tumors antagonizing p53-mediated apoptosis inflammation-induced cell migration nf-κb1-snail1 pathway represses nf-kappab activity dna damage-induced apoptosis variable β-catenin expression zeb1 represses e-cadherin double-negative feedback loop emt-activating transcription factors integrin-dependent nuclear translocation interleukin-dependent inflammatory network myc/mycn-activated microrna e-cadherin promotes metastasis epithelial-mesenchymal zeb1 links tumor-suppressive pten cernas tgfβ/bmp signaling pathway thrombin-induced tumor angiogenesis autocrine signals induce e-cadherin disrupts establishment e-cadherin repressors zeb1 gsk-3β-mediated phosphorylation e-cadherin repressor snail decreases zeb1-mediated emt elicit epithelial-mesenchymal transition hif-1α promotes metastasis epithelial-mesenchymal transition predicts e-cadherin gene expression zeb/mir-200 feedback loop smad-interacting protein-1 smad-interacting protein 1 repressing e-cadherin expression mir-200c mediate suppression hepatocellular carcinoma-derived cells twist-snail axis critical microrna-30a inhibits epithelial
Questions {❓}
- Brabletz S, Brabletz T (2010) The ZEB/miR-200 feedback loop—a motor of cellular plasticity in development and cancer?
- Franco HL, Casanovas J, Rodríguez-Medina JR, Cadilla CL (2011) Redundant or separate entities?
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headline:EMT-activating transcription factors in cancer: beyond EMT and tumor invasiveness
description:Cancer is a complex multistep process involving genetic and epigenetic changes that eventually result in the activation of oncogenic pathways and/or inactivation of tumor suppressor signals. During cancer progression, cancer cells acquire a number of hallmarks that promote tumor growth and invasion. A crucial mechanism by which carcinoma cells enhance their invasive capacity is the dissolution of intercellular adhesions and the acquisition of a more motile mesenchymal phenotype as part of an epithelial-to-mesenchymal transition (EMT). Although many transcription factors can trigger it, the full molecular reprogramming occurring during an EMT is mainly orchestrated by three major groups of transcription factors: the ZEB, Snail and Twist families. Upregulated expression of these EMT-activating transcription factors (EMT-ATFs) promotes tumor invasiveness in cell lines and xenograft mice models and has been associated with poor clinical prognosis in human cancers. Evidence accumulated in the last few years indicates that EMT-ATFs also regulate an expanding set of cancer cell capabilities beyond tumor invasion. Thus, EMT-ATFs have been shown to cooperate in oncogenic transformation, regulate cancer cell stemness, override safeguard programs against cancer like apoptosis and senescence, determine resistance to chemotherapy and promote tumor angiogenesis. This article reviews the expanding portfolio of functions played by EMT-ATFs in cancer progression.
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E-cadherin
EMT
Invasiveness
Metastasis
Snail1
Snail2
Tumorigenesis
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ZEB1
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Cell Biology
Biomedicine
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description:Cancer is a complex multistep process involving genetic and epigenetic changes that eventually result in the activation of oncogenic pathways and/or inactivation of tumor suppressor signals. During cancer progression, cancer cells acquire a number of hallmarks that promote tumor growth and invasion. A crucial mechanism by which carcinoma cells enhance their invasive capacity is the dissolution of intercellular adhesions and the acquisition of a more motile mesenchymal phenotype as part of an epithelial-to-mesenchymal transition (EMT). Although many transcription factors can trigger it, the full molecular reprogramming occurring during an EMT is mainly orchestrated by three major groups of transcription factors: the ZEB, Snail and Twist families. Upregulated expression of these EMT-activating transcription factors (EMT-ATFs) promotes tumor invasiveness in cell lines and xenograft mice models and has been associated with poor clinical prognosis in human cancers. Evidence accumulated in the last few years indicates that EMT-ATFs also regulate an expanding set of cancer cell capabilities beyond tumor invasion. Thus, EMT-ATFs have been shown to cooperate in oncogenic transformation, regulate cancer cell stemness, override safeguard programs against cancer like apoptosis and senescence, determine resistance to chemotherapy and promote tumor angiogenesis. This article reviews the expanding portfolio of functions played by EMT-ATFs in cancer progression.
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Cancer stem cells
E-cadherin
EMT
Invasiveness
Metastasis
Snail1
Snail2
Tumorigenesis
Twist1
Twist2
ZEB1
ZEB2
Cell Biology
Biomedicine
general
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Biochemistry
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