# Kalluri and Weinberg 2009: the basics of epithelial-mesenchymal transition

Source: https://onco.cc/key-papers/paper-kalluri-weinberg-emt-basics-jci-2009/  
OnCo record `paper-kalluri-weinberg-emt-basics-jci-2009` (Key paper). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

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.

## Summary

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.

## Fields

- Kind: Key paper
- Last checked: 2026-09-08
- Journal: Journal of Clinical Investigation
- Year: 2009
- DOI: 10.1172/JCI39104
- Authors: Kalluri R, Weinberg RA.
- Findings: EMT is classified into three types: developmental, fibrotic and cancer-associated (type 3).; Type 3 EMT gives carcinoma cells motility, invasiveness and resistance to apoptosis, and is driven by Snail, Slug, Twist and ZEB transcription factors downstream of TGF-beta and other signals.; The reverse process, mesenchymal-epithelial transition, is proposed to allow disseminated cells to form metastases.
- What it means: 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.
- Caveats: The extent to which full EMT occurs in human tumours in vivo, versus partial or hybrid states, is still debated.; A review; lineage-tracing evidence for EMT in metastasis came later and is mixed.

## Sources

- Full text (DOI): https://doi.org/10.1172/JCI39104

## Connected records

- key papers: [Lamouille 2014: molecular mechanisms of epithelial-mesenchymal transition](https://onco.cc/key-papers/paper-lamouille-emt-molecular-mechanisms-nrmcb-2014/), [Mani 2008: the epithelial-mesenchymal transition generates cells with properties of stem cells](https://onco.cc/key-papers/paper-mani-emt-stem-cell-properties-cell-2008/), [Thiery 2002: epithelial-mesenchymal transitions in tumour progression](https://onco.cc/key-papers/paper-thiery-emt-tumour-progression-nrc-2002/)
- pathways: [Epithelial-mesenchymal transition & drug efflux](https://onco.cc/pathways/emt/), [TGF-β signalling](https://onco.cc/pathways/tgf-beta/), [The metastatic cascade](https://onco.cc/pathways/metastatic-cascade/)
- terms: [Hallmark: activating invasion and metastasis](https://onco.cc/terms/activating-invasion-metastasis/), [Metastasis](https://onco.cc/terms/metastasis/)

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