Targeting EMT in cancer: Opportunities for pharmacological intervention

Felicity M. Davis, Teneale A. Stewart, Erik W. Thompson, Gregory R. Monteith

Research output: Contribution to journalReview articlepeer-review

233 Scopus citations


The spread of cancer cells to distant organs represents a major clinical challenge in the treatment of cancer. Epithelial-mesenchymal transition (EMT) has emerged as a key regulator of metastasis in some cancers by conferring an invasive phenotype. As well as facilitating metastasis, EMT is thought to generate cancer stem cells and contribute to therapy resistance. Therefore, the EMT pathway is of great therapeutic interest in the treatment of cancer and could be targeted either to prevent tumor dissemination in patients at high risk of developing metastatic lesions or to eradicate existing metastatic cancer cells in patients with more advanced disease. In this review, we discuss approaches for the design of EMT-based therapies in cancer, summarize evidence for some of the proposed EMT targets, and review the potential advantages and pitfalls of each approach.

Original languageEnglish (US)
Pages (from-to)479-488
Number of pages10
JournalTrends in Pharmacological Sciences
Issue number9
StatePublished - Sep 2014
Externally publishedYes

Bibliographical note

Funding Information:
This work was supported by the National Health and Medical Research Council (Project Grant 1022263) and the Queensland Cancer Council (1042819). E.W.T. was funded in part by the EMPathy National Collaborative Research Program of the National Breast Cancer Foundation, Australia. We thank Christine Chaffer for her valuable input into the MET section of this review.


  • Epithelial-mesenchymal transition (EMT)
  • cancer
  • cancer stem cells
  • invasion
  • mesenchymal-epithelial transition (MET)
  • metastasis
  • therapeutic targets
  • therapy resistance


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