File:Regulation of major EMT transcription factors by signalling pathways.jpg
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| Description | Figure 2 Regulation of major EMT transcription factors by signalling pathways. Epithelial-mesenchymal transition (EMT) is driven by SNAIL, zinc-finger E-box-binding (ZEB), and basic helix-loop-helix (bHLH) transcription factors that act as downstream effectors from several other signalling molecules. 1, Wnt signalling: WNT inhibits glycogen synthase kinase-3β (GSK3β) to stabilize β-catenin, which translocates to the nucleus to recruit the transcription factors; lymphoid enhancer-binding factor 1 (LEF) and T-cell factor (TCF) and promotes expression of SNAIL1 and SNAIL2. 2, Notch signalling: binding of a ligand (such as delta-like or jagged) with Notch receptors initiates the Notch signalling through the proteolytic cleavage by γ-secretase complex to release NICD. NICD then undergoes nuclear translocation to regulate the expression of target genes, including SNAIL, ZEB, and bHLH families. 3, Transforming growth factor-β (TGFβ) promotes EMT by acting at various strata; SMAD-mediated and non-SMAD signalling (i) SMAD-mediated signalling: Activation of the TβRI and TβRII turns on SMAD2 and SMAD3, which then integrate with SMAD4 to form a trimeric SMAD complex. This complex translocates into the nucleus to stimulate the expression of EMT transcription factors (ii) non-SMAD-mediated signalling: TGFβ also activates ERK through the RAS-MAKP pathway. Activated ERK can then stimulate the expression of SNAIL1 and SNAIL2 (unspecified in the image). 4–6, Growth factors (EGF, FGF, and HGF): various growth factors such as EGF, FGF, and PDGF activate receptor tyrosine kinases (RTKs), triggering dimerization and autophosphorylation of the intracellular domain of these receptors, which allows them to activate other downstream signalling molecules, including PI3K, PAK1, and STAT 3 and increase expression of SNAIL1 and SNAIL2. 7, Oestrogen; oestrogen is one of the few molecular candidates that negatively regulate EMT. It does this through direct inhibition of Slug transcription by forming a co-repressor complex consisting of ligand-activated ERα, HDAC1, and nuclear receptor co-repressor (NCoR) that binds to the oestrogen-response elements at the slug promoter sequence and inhibit its expression. 8, Hypoxia: in normoxic conditions, prolyl hydroxylases are activated which causes hydroxylation of HIF-1α and thereby hindering their activities, whereas, hypoxia stabilizes the enzymes, enabling their nuclear translocation and heterodimerization and binding to oversee stimulation of Twist and stabilization of SNAIL1/2. 9, Tumour necrotic factor-alpha (TNF-α): TNF-α signal activates IKB kinase complex (IKK), which in turn phosphorylates NF-kB inhibitor. Consequently, NF-kB becomes active and undergoes nuclear translocation to promote induction of Twist1 expression. |
| Date | |
| Source | https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2021.762817/full Understanding the Complex Milieu of Epithelial-Mesenchymal Transition in Cancer Metastasis: New Insight Into the Roles of Transcription Factors. Front. Oncol. 11:762817. doi: 10.3389/fonc.2021.762817 |
| Author | Imodoye SO, Adedokun KA, Muhammed AO, Bello IO, Muhibi MA, Oduola T and Oyenike MA |
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Copyright © 2021 Imodoye, Adedokun, Muhammed, Bello, Muhibi, Oduola and Oyenike. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
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| current | 10:07, 19 May 2024 | | 3,828 × 4,004 (1.42 MB) | Rasbak (talk | contribs) | {{Information |description=Figure 2 Regulation of major EMT transcription factors by signalling pathways. Epithelial-mesenchymal transition (EMT) is driven by SNAIL, zinc-finger E-box-binding (ZEB), and basic helix-loop-helix (bHLH) transcription factors that act as downstream effectors from several other signalling molecules. 1, Wnt signalling: WNT inhibits glycogen synthase kinase-3β (GSK3β) to stabilize β-catenin, which translocates to the nucleus to recruit the transcription factors; lymp... |
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