Loading
The detailed molecular account of how cells switch from a fixed epithelial state to a mobile mesenchymal one, from the TGF-beta signals that start it to the transcription factors, microRNAs and cytoskeletal changes that carry it out.
Lamouille, Xu and Derynck reviewed the machinery of epithelial-mesenchymal transition: TGF-beta signalling through SMAD and non-SMAD routes as the best-characterised trigger, the core transcription factors Snail, ZEB and Twist that repress E-cadherin and epithelial genes, the miR-200 and miR-34 families that hold those factors in check, and the changes in junctions, polarity and actin cytoskeleton that produce motility and invasion. They stressed that EMT is often partial and reversible, with cells occupying intermediate states, and described how the programme is co-opted in fibrosis and cancer.
This is the reference for the mechanics behind invasion and metastasis and for why partial EMT states, rather than a full switch, are now thought to matter most in cancer. It also explains the appeal and the difficulty of drugging EMT, since its drivers are transcription factors.
Shares Kalluri and Weinberg 2009: the basics of epithelial-mesenchymal transition, Metastasis, TGF-β signalling, Epithelial-mesenchymal transition & drug efflux.
Shares Hallmark: activating invasion and metastasis, Metastasis.
Shares Hallmark: activating invasion and metastasis, Metastasis, Epithelial-mesenchymal transition & drug efflux.
Shares Hallmark: activating invasion and metastasis, Metastasis.
Shares Thiery 2002: epithelial-mesenchymal transitions in tumour progression, Kalluri and Weinberg 2009: the basics of epithelial-mesenchymal transition, Hallmark: activating invasion and metastasis, Metastasis.
Shares Hallmark: activating invasion and metastasis, Metastasis.
Shares Hallmark: activating invasion and metastasis, Metastasis, TGF-β signalling.
Shares TGF-β signalling, Epithelial-mesenchymal transition & drug efflux.