The Publication:

Emodin Inhibits Breast Cancer Growth by Blocking the Tumor-Promoting Feedforward Loop between Cancer Cells and Macrophages

Sounds like a mouthful? Don’t worry—there’s a summary below.

Publication Summary:

In breast cancer patients, the more macrophages, a type of immune cells, are in the tumors, the more severe is the cancer. Cancer cells recruit macrophages and educate them to adopt a pro-tumor M2-like phenotype through the secretion of molecules such as MCP1 and CSF1. Macrophages in turn promote tumor growth through supporting new vessel formation in the tumors, weakening immune response against cancer cells, remodelingextracellular matrix, and promoting cancer cell migrationout of the tumors. Thus, tumor cells and macrophages interact to create a feedforward loop supporting tumor growth and spread (metastasis). In this study, we assessed the ability of emodin, a Chinese herb-derived compound, to inhibit breast cancer growth in mice and examined the underlying mechanisms. Emodin was used to treat mice bearing breast tumors. It was shown that emodin suppressed tumor growth by reducingmacrophage number in the tumors and their M2-like polarization, accompanied by increased cancer cell-killing immune cells (called T-cells) and reduced new vessel formation in tumors. Mechanistical study revealed that emodin inhibits macrophage infiltration and M2-like polarization by altering the activation of several transcription factors and the histone modifications. These results suggest that emodin acts on both breast cancer cells and macrophages and effectively blocks the tumor-promoting feedforward loop between the two cell types, thereby inhibiting breast cancer growth and metastasis.