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Review
. 2019 Jan 3;24(1):65-78.
doi: 10.1016/j.stem.2018.11.011. Epub 2018 Dec 13.

Phenotypic Plasticity: Driver of Cancer Initiation, Progression, and Therapy Resistance

Piyush B Gupta  1 , Ievgenia Pastushenko  2 , Adam Skibinski  3 , Cedric Blanpain  4 , Charlotte Kuperwasser  5
Affiliations
Review

Phenotypic Plasticity: Driver of Cancer Initiation, Progression, and Therapy Resistance

Piyush B Gupta et al. Cell Stem Cell. .

Abstract

Our traditional understanding of phenotypic plasticity in adult somatic cells comprises dedifferentiation and transdifferentiation in the context of tissue regeneration or wound healing. Although dedifferentiation is central to tissue repair and stemness, this process inherently carries the risk of cancer initiation. Consequently, recent research suggests phenotypic plasticity as a new paradigm for understanding cancer initiation, progression, and resistance to therapy. Here, we discuss how cells acquire plasticity and the role of plasticity in initiating cancer, cancer progression, and metastasis and in developing therapy resistance. We also highlight the epithelial-to-mesenchymal transition (EMT) and known molecular mechanisms underlying plasticity and we consider potential therapeutic avenues.

Keywords: cancer; epithelial to mesenchymal transition; plasticity; therapy resistance.

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Figures

Figure 1.
Figure 1.. Types of Differentiation that Are Induced during Cellular Plasticity.
Types of epithelial differentiation and plasticity seen in the mammary gland and how it relates to more primitive states of multipotency seen during embryonic development.
Figure 2.
Figure 2.. Tumor Transition States Occurring during EMT.
(A–D) Changes in cell morphology (A), gene expression (B), chromatin remodeling (C), and transcription factors (D) involved in the regulation of different tumor transition states occurring during EMT.
See this image and copyright information in PMC

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