Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages

Figure 8

The schema of possible mechanism of chemoprevention of aspirin. In 4T1 breast cancer cell environment, RAW264.7 macrophage infiltration increased VEGF, PAI-1, TNF-α, IL-6, and TGF-β levels, and M2 macrophage expression, resulting to, benefit to tumor progression. Aspirin treatment decreased angiogenic and inflammation-associated cytokine VEGF, PAI-1, MCP-1, IL-6, IL-10, and TGF-β production. In addition, treatment of aspirin increased M1 expression and decreased M2 expression in macrophages, resulting to interference of the communication in this microenvironment and blunted tumor progression.