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The standard primer on how cancer cells borrow a programme from embryonic development to loosen their attachments, become mobile and invade, and how the same programme also drives wound healing and organ scarring.
Kalluri and Weinberg organised the epithelial-mesenchymal transition (EMT) into three types: type 1 in embryonic development, type 2 in wound healing and fibrosis, and type 3 in cancer, where carcinoma cells at the invasive front lose E-cadherin and epithelial polarity, gain mesenchymal markers such as vimentin and N-cadherin, and acquire motility and invasiveness. They summarised the transcription factors that drive it (Snail, Slug, Twist, ZEB1 and ZEB2), the signals that trigger it (TGF-beta, Wnt, Notch and growth factor receptor pathways) and the reverse transition that lets disseminated cells re-form epithelial metastases.
EMT is the most cited explanation for how carcinomas invade and spread and for part of their drug resistance. This primer is the entry point for the field, and its framework informs current work on partial EMT states, circulating tumour cells and therapies aimed at the transition.
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.
This paper is why metastasis, stemness and therapy resistance are now studied as one problem. It suggests that the cells most able to spread are also the ones most able to regrow, and it motivates therapies that target the mesenchymal or stem-like state.
This is the paper that made EMT a cancer concept, cited by almost every metastasis study since. It set the research agenda that later produced the EMT stem cell link and current work on partial EMT states.
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 Hallmark: activating invasion and metastasis, Metastasis, The metastatic cascade.
Shares Metastasis, The metastatic cascade.
Shares The metastatic cascade, TGF-β signalling.
Shares Hallmark: activating invasion and metastasis, Metastasis, The metastatic cascade, TGF-β signalling.
Shares Hallmark: activating invasion and metastasis, The metastatic cascade, TGF-β signalling, Epithelial-mesenchymal transition & drug efflux.