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View full-text article in PMC

. 2017 Jul 4;9(7):77. doi: 10.3390/cancers9070077

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© 2017 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Schematic of epithelial-to-pericyte transition (EPT). In response to microenvironmental stimuli (e.g., hypoxia, transforming growth factor β TGFβ), a subset of carcinoma cells in the tumor mass undergo EMT, and consequently acquire increased motility and invasiveness as well as expression of PDGFRβ, N-cadherin, and other pericyte markers. As endothelial cells express N-cadherin and secrete PDGF, the EMT cancer cells are chemoattracted to vasculature via PDGF paracrine signaling and associate with endothelial cells through N-cadherin-mediated adherens junctions. The EMT cells may also upregulate CXCR4 and be recruited to endothelium in response to stromal-derived factor 1 (SDF1). Due to lack of PDGFRβ and N-cadherin, epithelial cancer cells without EMT are unable to respond to PDGF or interact with endothelium. The EMT cancer cells functionally resemble pericytes to stabilize blood vessels to fuel tumor growth.