The Publication:

Emodin Reduces Breast Cancer Lung Metastasis by Suppressing Macrophage-induced Breast Cancer Cell Epithelial-mesenchymal Transition and Cancer Stem Cell Formation

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

Publication Summary:

Cancer is known for being very clever. While your immune system works very hard to fight off and kill cancer cells before they can multiply, cancer has learned how to evade your immune system’s attacks, and sometimes even make it help the cancer grow and spread. There are many types of immune cells. One type of immune cell is known as macrophages, which “kill” cancer cells. However, cancer cells are known to take these macrophages and re-train them to help cancer cells instead of killing them. Cancer-killing macrophages, or “good” macrophages are called anti-tumor macrophages, whereas cancer-promoting macrophages are called pro-tumor macrophages. One way that cancer cells do this is that they utilize the protein TGF-beta1, which turns macrophages into pro-tumor ones. Macrophages are a key component of cancer spread and proliferation, and so finding treatments that keep cancer from hijacking these immune cells is crucial.

In this study, we examined how the natural product emodin influences macrophages and TGF-beta1 in respect to cancer growth. We found that giving emodin before surgery for the removal of breast tumors (known as neoadjuvant therapy) resulted in lower rates of cancer lung metastasis due to the emodin treatment reducing the number of pro-tumor macrophages in tumors. It was revealed that emodin did this by stopping TGF-beta1 signaling in breast cancer cells, therefore keeping the protein from helping the cancer grow. This also allows anti-tumor macrophages to keep doing their job and kill cancer cells. Because of these effects, we believe that emodin can be a powerful tool for treating—and even preventing—breast cancer growth and development.

Written and illustrated by Kaylie Lively