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Cancer October 10, 2018

"Invadopodia" key to spread of breast cancer cells, Stanford researchers find

By Krista Conger

Stanford researchers have learned that cancer cells can batter their way into new territory, rather than relying on dissolving chemicals.

I was consumed with envy when I read this Stanford Engineering article by my colleague Tom Abate about how breast cancer cells spread. Tom was reporting about research from the laboratory of mechanical engineer Ovijit Chaudhuri, PhD. Chaudhuri, together with former graduate student Katrina Wisdom, found that the cells actually punch their way through surrounding normal tissue using protrusions called invadopodia. (Am I the only one who can't read that without hearing a corny, spooky Halloween voice? In-VAY-do PODIA! Ahem.)

The research, which was conducted by embedding breast cancer cells within a specially constructed, gelatin-like biogel, was recently published in Nature Communications. The findings provide a counterpoint to a previously held belief that invadopodia rely exclusively on secretions of chemicals called proteases to burn through the surrounding membrane that serves as a natural barrier between tissues. Once breached, the membrane allows cells to squeeze through and invade other tissues. However, the biogel Wisdom constructed was impervious to protease secretions.

As the article states:

As it turned out, the cells could burrow through the gel. The time-lapse microscopy revealed how. Wisdom said the images show that cancer cells used their invadopodia like stiff arms to tear tiny holes in the biogel. Time and again the cancer cell formed and retracted its invadopodia until the repeated physical battering created an opening large enough for the entire cancer cell to scoot through.

The researchers put together this short animation to show how the cells move through the tissue.

Understanding how cancer cells invade can provide important clues about how to stop them. The fact that the invadopodia can use physical force to burrow through tissues might explain why drugs that work to inhibit the activity of proteases haven't been particularly effective at preventing metastases, the researchers said.

Photo by Tom Coates

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Krista-Conger

Science writer

Krista Conger

Senior science writer Krista Conger, PhD ’99, covers cancer, stem cells, dermatology, developmental biology, endocrinology, pathology, hematology, radiation oncology and LGBTQ+ issues for the office. She received her undergraduate degree in biochemistry at the University of California, Berkeley and her PhD in cancer biology from Stanford University. After completing the science writing program at UC Santa Cruz, she joined the Stanford Medicine Office of Communications in 2000. She enjoys distilling complicated scientific topics into engaging prose accessible to the layperson. Over the years, she has had chronicled nascent scientific discoveries from their inception to Food and Drug Administration approval and routine clinical use — documenting the wonder and long arc of medical research. Her writing has repeatedly been recognized with awards from the Counsel for the Advancement and Support of Education and the Association of American Medical Colleges. She is a member of the National Academy of Science Writers and a certified science editor through the Board of Editors in the Life Sciences. In her spare time, she enjoys textile arts, experimenting with new recipes and hiking in beautiful northwestern Montana, where she was raised and now lives.