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Targeting EMT in cancer: opportunities for pharmacological intervention.

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Affiliations

  • 1. School of Pharmacy, The University of Queensland, Brisbane, QLD, Australia.
      Authors
    • Davis FM 1
    • Stewart TA 1
    • Monteith GR 1
    (3 authors)
  • 2. St. Vincent's Institute, Fitzroy, VIC, Australia; University of Melbourne Department of Surgery, St Vincent's Hospital, Fitzroy, VIC, Australia; Institute of Health and Biomedical Innovation, Queensland Institute of Technology, Kelvin Grove, QLD, Australia.
      Authors
    • Thompson EW 2
    (1 author)

ORCIDs linked to this article

Trends in Pharmacological Sciences, 16 Jul 2014, 35(9):479-488
https://doi.org/10.1016/j.tips.2014.06.006 PMID: 25042456 

Review

A comment on this article appears in "Voltage-gated sodium channel blockade for inhibition of EMT." Trends Pharmacol Sci. 2014 Dec;35(12):621.

Abstract 

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.

Full text links 

Read article at publisher's site: https://doi.org/10.1016/j.tips.2014.06.006

Read article for free, from open access legal sources, via Unpaywall: https://eprints.qut.edu.au/88684/1/Targeting%20EMT%20in%20cancer.pdfUnpaywall

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