Blocking Dab2 Could Stop Cancer Spread

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Around 85% of all tumours are epithelial in origin and have epithelial markers on the cell surfaces. In breast, ovarian, pancreatic and colon-rectal cancers, metastasis – when cells break away from the primary tumour to initiate a new tumour elsewhere in the body – is often fatal. A process known as epithelial-mesenchymal transdifferentiation (EMT) plays a role in releasing epithelial cells from the surface of solid tumours and transforming them into transient mesenchymal cells which have reduced cell-cell adhesion properties and increased ability to migrate and establish new tumours. It was already known that transforming growth factor-β (TGF-β) induces EMT but the downstream events were unclear.

Scientists in the US have now shown that TGF-β triggers the formation of a protein known as disabled-2 (Dab2) which, in turn, activates the EMT process. An increased understanding of the signalling pathway for modulating EMT could lead to the design of drugs to delay or halt EMT and control tumour metastasis. The discovery may also help to understand the progression of other diseases.

The study is published in Nature Cell Biology.

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