Researchers pinpoint path to breast cancer metastasis

The Weinberg lab has identified signaling pathways that prompt breast cancer cells to spread. Blocking these pathways could offer an approach for preventing breast cancer metastasis.

Epithelial and mesenchymal cells

During epithethial-to-mesenchymal transition (EMT), static, tightly packed epithelial cells (highlight in red with blue nucleui) acquire the traits of freely moving, loose mesenchymal cells (highlighted in green with blue nuclei).

In order to leave a primary tumor, breast cancer cells must undergo a process known as EMT or epithethial-to-mesenchymal transition. In this transition, the cells convert from static, tightly packed cells to freely moving, loose cells, allowing them to roam around the body and form new tumors elsewhere.

But what causes the cancer cells to undergo EMT? Christina Scheel, a postdoctoral researcher in Bob Weinberg’s lab, discovered signaling pathways—in which specific molecules act to influence cell function—that jump-start the process. The signals are part of normal cell behavior, but cancer cells can hijack them and use them for their own benefit.

Scheel theorized that if cancer cells couldn’t hijack the signals, they couldn’t undergo EMT, thereby preventing the spread of the cancer. To test this theory, she treated mice carrying a model of human breast cancer with proteins that block the signals in question. The result: the mouse with impaired signaling had 1/10 the number of tumors compared with the untreated mouse.

These findings offer new insight into how breast cancer cells exploit the body’s own systems, with deleterious consequences, and may offer a novel approach to reducing or even preventing breast cancer metastasis in humans.

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