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  • ISSN 1674-8301
  • CN 32-1810/R
Volume 32 Issue 2
Feb.  2018
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Andrew Sulaiman, Zemin Yao, Lisheng Wang. Re-evaluating the role of epithelial-mesenchymal-transition in cancer progression[J]. The Journal of Biomedical Research, 2018, 32(2): 81-90. DOI: 10.7555/JBR.31.20160124
Citation: Andrew Sulaiman, Zemin Yao, Lisheng Wang. Re-evaluating the role of epithelial-mesenchymal-transition in cancer progression[J]. The Journal of Biomedical Research, 2018, 32(2): 81-90. DOI: 10.7555/JBR.31.20160124
shu

Re-evaluating the role of epithelial-mesenchymal-transition in cancer progression

  • 1.

    Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Canada

  • 2.

    China-Canada Centre of Research for Digestive Diseases

  • 3.

    Ottawa Institute of Systems Biology, University of Ottawa, 451 Smyth Road, Ottawa, Ontario K1H 8M5, Canada

  • 4.

    Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario K1H 8L6, Canada.

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We thank Dr. Luk Cox and Dr. Idoya Lahortiga from Somersault 18:24 to allow the use of their Library of Science and Medical Illustrations (http:// www.somer- 86 Sulaiman A et al. J Biomed Res, 2018,32(2)sault1824.com/resources/) for the creation of the Fig. 1. This work is supported by operating grants from Canadian Breast Cancer Foundation-Ontario Region and the Canadian Institutes of Health Research MOP- 111224 to LW.

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  • Received Date: September 27, 2016
  • Revised Date: October 30, 2016
    Graphical Abstract
    • Abstract
  • Epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) are essential for embryonic development and also important in cancer progression. In a conventional model, epithelial-like cancer cells transit to mesenchymal-like tumor cells with great motility via EMT transcription factors; these mesenchymallike cells migrate through the circulation system, relocate to a suitable site and then convert back to an epithelial-like phenotype to regenerate the tumor. However, recent findings challenge this conventional model and support the existence of a stable hybrid epithelial/mesenchymal (E/M) tumor population. Hybrid E/M tumor cells exhibit both epithelial and mesenchymal properties, possess great metastatic and tumorigenic capacity and are associated with poorer patient prognosis. The hybrid E/M model and associated regulatory networks represent a conceptual change regarding tumor metastasis and organ colonization. It may lead to the development of novel treatment strategies to ultimately stop cancer progression and improve disease-free survival.
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    1. Tsai CY, Ko HJ, Chiou SJ, et al. GSKIP modulates cell aggregation through EMT/MET signaling rather than differentiation in SH-SY5Y human neuroblastoma cells. J Cell Commun Signal, 2023. DOI:10.1007/s12079-023-00752-z. Online ahead of print
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