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. 2021 Feb 24;13(5):942. doi: 10.3390/cancers13050942

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© 2021 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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General outline for the action of EP4 antagonists used in breast cancer treatment (right panel) compared to conditions of no treatment (left panel). The diagram includes the interaction of EP4 agonist PGE2 with EP4 receptors on sprouting endothelial cells (tip cells), natural killer (NK) cells and macrophages, along with VEGFs binding to VEGF receptors (VEGFRs) located on the tip cells of newly formed lymphatics (green) and blood vessels (red). VEGFs are released by hypoxia induction within the tumor core (black cells). Also, the presence of matrix metalloproteases (MMPs) enhances tip cell invasion into the extracellular matrix to complete vasculature. The right panel demonstrates how EP4-antagonist treatment abrogates both angiogenesis and lymphangiogenesis. Furthermore, EP4 antagonist treatment prevents the stimulation of cancer stem-like cells (SLCs) in breast cancer. Lastly, antagonizing EP4 receptors located on various immune cells (NK cell and macrophages) allow an enhanced anti-tumor immune response.