
DOI . ORG {
}
Title[redir]:
Epithelial-mesenchymal transition orchestrates tumor microenvironment: current perceptions and challenges | Journal of Translational Medicine | Full Text
Description:
The epithelial-mesenchymal transition (EMT) is a critical process in cancer progression, facilitating tumor cells to develop invasive traits and augmenting their migratory capabilities. EMT is primed by tumor microenvironment (TME)-derived signals, whereupon cancer cells undergoing EMT in turn remodel the TME, thereby modulating tumor progression and therapeutic response. This review discusses the mechanisms by which EMT coordinates TME dynamics, including secretion of soluble factors, direct cell contact, release of exosomes and enzymes, as well as metabolic reprogramming. Recent evidence also indicates that cells undergoing EMT may differentiate into cancer-associated fibroblasts, thereby establishing themselves as functional constituents of the TME. Elucidating the relationship between EMT and the TME offers novel perspectives for therapeutic strategies to enhance cancer treatment efficacy. Although EMT-directed therapies present significant therapeutic potential, the current lack of effective targeting approachesāattributable to EMT complexity and its microenvironmental context dependencyāunderscores the necessity for mechanistic investigations and translational clinical validation.
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Keywords {š}
pubmed, cancer, article, cells, google, scholar, emt, cell, cas, central, tumor, immune, expression, pdl, transition, breast, zeb, tme, mesenchymal, epithelialmesenchymal, signaling, ecm, extracellular, wang, nat, metastasis, collagen, carcinoma, snail, metabolic, progression, promotes, immunol, epithelial, ecadherin, liu, target, function, process, targeting, vimentin, receptor, res, chen, activation, matrix, tgfβ, inhibition, therapeutic, immunosuppressive,
Topics {āļø}
fgd5-as1/mir-454-3p/zeb1-vegf axis apkc-ι/snail-induced cca cells ccl18-zeb1-m-csf feedback loop mir-30-5p/snail/dpp4 axis ccr5-dependent t-cell retention grhl2/zeb1/pd-l1 axis tgf-β-mediated myofibroblastic differentiation tgf-β1-induced emt resulted double-negative feedback loop pro-angiogenic cd14+/kdr+ population virus counteracts mir-200c regulating pd-1/pd-l1 checkpoint pd-l1-mediated emt induction anti-erbb2 monoclonal antibody microrna-200/zeb1 axis control tumor-specific tumor-infiltrating lymphocytes pd-l1 prominently activates mirna-rich exosome delivery tumor necrosis factor-α lox/hypoxia axis reverses downstream phospho-cascades triggers mir-199a-5p loss piezo1-yap signalling axis loxl2-mediated metastatic cascade emt-driven pd-l1 upregulation cell-cell contacts mediated additional information publisher' pd-l1 induces epithelial single-cell rna sequencing positive feedback loop enhanced gm-csf production hypoxia-induced lysyl oxidase pd-1/pd-l1 signaling [52] promotes anti-tumor immunity binary epithelial/mesenchymal paradigm transforming growth factor-β emt-selective inhibitors exist single emt-tf recapitulate inhibitory c-type lectin delivering mir-21-abundant exosomes potentiating anti-tumor immunity lactate-induced ph reduction her2/erbb2 antibody therapy pd-l1-mediated immunosuppression her2-positive breast cancer enhance t-cell function pd-1/pd-l1 checkpoint induces cd4+foxp3+ regulatory increased pd-l1 expression jnk/c-jun activation
Questions {ā}
- T cell adhesion and cytolysis of pancreatic cancer cells: A role for E-cadherin in immunotherapy?
- While EMT-TFs are indeed crucial initiators of the process, can the upregulation of a single EMT-TF recapitulate the pathophysiological EMT spectrum in vivo?
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headline:Epithelial-mesenchymal transition orchestrates tumor microenvironment: current perceptions and challenges
description:The epithelial-mesenchymal transition (EMT) is a critical process in cancer progression, facilitating tumor cells to develop invasive traits and augmenting their migratory capabilities. EMT is primed by tumor microenvironment (TME)-derived signals, whereupon cancer cells undergoing EMT in turn remodel the TME, thereby modulating tumor progression and therapeutic response. This review discusses the mechanisms by which EMT coordinates TME dynamics, including secretion of soluble factors, direct cell contact, release of exosomes and enzymes, as well as metabolic reprogramming. Recent evidence also indicates that cells undergoing EMT may differentiate into cancer-associated fibroblasts, thereby establishing themselves as functional constituents of the TME. Elucidating the relationship between EMT and the TME offers novel perspectives for therapeutic strategies to enhance cancer treatment efficacy. Although EMT-directed therapies present significant therapeutic potential, the current lack of effective targeting approachesāattributable to EMT complexity and its microenvironmental context dependencyāunderscores the necessity for mechanistic investigations and translational clinical validation.
datePublished:2025-04-02T00:00:00Z
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description:The epithelial-mesenchymal transition (EMT) is a critical process in cancer progression, facilitating tumor cells to develop invasive traits and augmenting their migratory capabilities. EMT is primed by tumor microenvironment (TME)-derived signals, whereupon cancer cells undergoing EMT in turn remodel the TME, thereby modulating tumor progression and therapeutic response. This review discusses the mechanisms by which EMT coordinates TME dynamics, including secretion of soluble factors, direct cell contact, release of exosomes and enzymes, as well as metabolic reprogramming. Recent evidence also indicates that cells undergoing EMT may differentiate into cancer-associated fibroblasts, thereby establishing themselves as functional constituents of the TME. Elucidating the relationship between EMT and the TME offers novel perspectives for therapeutic strategies to enhance cancer treatment efficacy. Although EMT-directed therapies present significant therapeutic potential, the current lack of effective targeting approachesāattributable to EMT complexity and its microenvironmental context dependencyāunderscores the necessity for mechanistic investigations and translational clinical validation.
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