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Angiocrine factors modulate tumor proliferation and motility through EphA2 repression of Slit2 tumor suppressor function in endothelium
Journal article   Open access   Peer reviewed

Angiocrine factors modulate tumor proliferation and motility through EphA2 repression of Slit2 tumor suppressor function in endothelium

Dana M. Brantley-Sieders, Charlene M. Dunaway, Meghana Rao, Sarah Short, Yoonha Hwang, Yandong Gao, Deyu Li, Aixiang Jiang, Yu Shyr, Jane Y. Wu, …
Cancer research (Chicago, Ill.), Vol.71(3), pp.976-987
02/01/2011
DOI: 10.1158/0008-5472.CAN-10-3396
PMCID: PMC3032824
PMID: 21148069
url
https://doi.org/10.1158/0008-5472.CAN-10-3396View
Published (Version of record) Open Access

Abstract

It is well known that tumor-derived pro-angiogenic factors induce neovascularization to facilitate tumor growth and malignant progression. However, the concept of `angiocrine' signaling, in which signals produced by endothelial cells elicit tumor cell responses distinct from vessel function has been proposed, yet remains under investigated. Here, we report that angiocrine factors secreted from endothelium regulate tumor growth and motility. We found that Slit2, which is negatively regulated by endothelial EphA2 receptor, is one such tumor suppressive angiocrine factor. Slit2 activity is elevated in EphA2-deficient endothelium. Blocking Slit activity restored angiocrine-induced tumor growth/motility, whereas elevated Slit2 impaired growth/motility. To translate our findings to human cancer, we analyzed EphA2 and Slit2 expression in human cancer. EphA2 expression inversely correlated with Slit2 in the vasculature of invasive human ductal carcinoma samples. Moreover, analysis of large breast tumor datasets revealed that Slit2 correlated positively with overall and recurrence-free survival, providing clinical validation for the tumor suppressor function for Slit2 in human breast cancer. Together, these data support a novel, clinically relevant mechanism through which EphA2 represses Slit2 expression in endothelium to facilitate angiocrine-mediated tumor growth and motility by blocking a tumor suppressive signal.
angiocrine signaling breast cancer endothelium EphA2 Slit2

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