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Cancer biology

TGFβ and EMT as double agents

Nature Reviews Molecular Cell Biology volume 17, pages 202–203 (2016)Cite this article

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To study the duality of TGFβ signalling, the authors investigated the tumour-forming properties of mouse pancreatic cancer cells exposed to TGFβ. They observed that TGFβ signalling-competent cells, in contrast to signalling-deficient cells, did not show oncogenic properties. Interestingly, the signalling-competent cells displayed phenotypes characteristic of EMT and underwent apoptosis following TGFβ treatment, and live-cell microscopy revealed that EMT preceded apoptosis. RNA sequencing provided further evidence that TGFβ indeed induces EMT, as increased expression of the EMT driver Snail was observed. Notably however, overexpression of Snail alone was insufficient to induce apoptosis, indicating that TGFβ provides additional inputs, as well as EMT induction, that are necessary for the execution of cancer cell apoptosis.

A candidate for further investigation of TGFβ-mediated apoptotic response was the transcription factor SOX4, which was strongly upregulated and required for apoptosis following TGFβ treatment. SOX4 supported apoptosis by inducing the expression of pro-apoptotic genes, but, interestingly, it was also demonstrated to be an important promoter of tumorigenesis, and its expression was shown to be required for cancer growth both in vitro and in vivo.

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References

  1. David, C. J. et al. TGF-β tumor suppression through a lethal EMT. Cell http://dx.doi.org/10.1016/j.cell.2016.01.009 (2016)

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  1. Paulina Strzyz
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Lamouille, S., Xu, J. & Derynck, R. Molecular mechanisms of epithelial–mesenchymal transition. Nat. Rev. Mol. Cell Biol. 15, 178–196 (2014)

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Strzyz, P. TGFβ and EMT as double agents. Nat Rev Mol Cell Biol 17, 202–203 (2016). https://doi.org/10.1038/nrm.2016.26

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