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Review
. 2020 Oct;30(10):764-776.
doi: 10.1016/j.tcb.2020.07.003. Epub 2020 Aug 13.

EMT, MET, Plasticity, and Tumor Metastasis

Affiliations
Review

EMT, MET, Plasticity, and Tumor Metastasis

Basil Bakir et al. Trends Cell Biol. 2020 Oct.

Abstract

Cancer cell identity and plasticity are required in transition states, such as epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET), in primary tumor initiation, progression, and metastasis. The functional roles of EMT, MET, and the partial state (referred to as pEMT) may vary based on the type of tumor, the state of dissemination, and the degree of metastatic colonization. Herein, we review EMT, MET, pEMT, and plasticity in the context of tumor metastasis.

Keywords: EMT; MET; cellular plasticity; colonization; metastasis; pEMT.

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Figures

Figure 1:
Figure 1:. Primary tumor cells undergo intravasation into the lymphatic-vascular systems.
There are multiple mechanisms by which tumor cells (blue rectangles) are thought to detach from the primary site and intravasate into the lymphatic-vascular systems. One proposed mechanism is complete EMT or cEMT (green spheres), whereby cells lose epithelial markers and gain mesenchymal characteristics. During partial EMT or pEMT, cells retain some of their epithelial characteristics. Another possibility is that cells undergoing EMT represent only a small portion of the total population that ultimately metastasize.
Figure 2:
Figure 2:. Primary tumor cells undergo extravasation and metastatic colonization.
Evidence in multiple model systems demonstrates that macrometastases have strong expression of epithelial markers (blue), which are likely a requirement for expansion within the metastatic site. One model suggests cells that previously underwent cEMT or pEMT regain epithelial markers and lose mesenchymal characteristics (green). Lastly, in mixed populations of metastatic cells, it is thought that the clusters of epithelial cells are the exclusive or dominant population capable of expanding and forming macrometastases.

References

    1. Mills JC et al. (2019) Nomenclature for cellular plasticity: are the terms as plastic as the cells themselves? EMBO J. 38 - PMC - PubMed
    1. Gupta PB et al. (2019) Phenotypic Plasticity: Driver of Cancer Initiation, Progression, and Therapy Resistance. Cell Stem Cell, 24, 65–78 - PMC - PubMed
    1. Polyak K and Weinberg RA (2009) Transitions between epithelial and mesenchymal states: Acquisition of malignant and stem cell traits. Nature Reviews Cancer, 9, 265–273 - PubMed
    1. Dongre A and Weinberg RA (2019) New insights into the mechanisms of epithelial–mesenchymal transition and implications for cancer. Nat. Rev. Mol. Cell Biol. 20, 69–84 - PubMed
    1. Pastushenko I and Blanpain C (2019) EMT Transition States during Tumor Progression and Metastasis. Trends in Cell Biology, 29, 212–226 - PubMed

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