EMT, MET, Plasticity, and Tumor Metastasis

Basil Bakir; Anna M Chiarella; Jason R Pitarresi; Anil K Rustgi

doi:10.1016/j.tcb.2020.07.003

EMT, MET, Plasticity, and Tumor Metastasis

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

Authors

Basil Bakir¹, Anna M Chiarella², Jason R Pitarresi¹, Anil K Rustgi³

Affiliations

¹ Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA 19104, USA.
² Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA.
³ Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY 10032, USA. Electronic address: [email protected].

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.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

MeSH terms

Animals
Cell Plasticity*
Disease Models, Animal
Epithelial-Mesenchymal Transition*
Humans
Models, Biological
Neoplasm Metastasis
Neoplasms / pathology*

Abstract

Publication types

MeSH terms

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