Revealing a Key Player in Cancer Metastasis

Invadopodia
A newly designed fluorescent biosensor shows where Rac1, a molecule involved in cancer metastasis, is active in this cell. Warmer colors show greater Rac1 activity. Credit: Yasmin Moshfegh, Albert Einstein College of Medicine.

Most of the more than half-a-million deaths caused by cancer each year in the United States result not from the original tumor but from the spread of cancer to new parts of the body, or metastasis. Cancer cells travel from a primary tumor using invadopodia, foot-like protrusions that break through surrounding connective tissue. Invadopodia are driven by protein filaments that repeatedly grow and disassemble. Exactly what guides this cycle was unclear, but scientists suspected a molecule called Rac1 might be involved. A new tool now sheds light on the details.

Researchers led by Louis Hodgson of Albert Einstein College of Medicine developed a fluorescent biosensor that glows wherever Rac1 is active in a cell, and they used it to study highly invasive breast cancer cells taken from rodents and humans. The scientists observed invadopodia form when Rac1 activity was low and disappear when it was high. They then confirmed their findings when they shut down the gene that encodes Rac1 and saw the invadopodia remain intact indefinitely.

This discovery suggests that targeting Rac1 activity with drugs could stop the spread of cancer cells. But a major hurdle remains: Healthy cells, including those that make up our immune system, also rely on the molecule for normal activity. Researchers must find a way to turn off Rac1 in cancer cells without disrupting its function in the rest of the body.

This work also was funded by NIH’s National Cancer Institute.

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Good Vibrations

A knot-like structure in a section of RNA from a flavivirus
Findings in mice may lead to a drug-free, noninvasive way to treat chronic wounds in people with type 2 diabetes. Credit: Stock image.

For people living with type 2 diabetes, wounds often heal slowly, sometimes even becoming chronic. Now, scientists have shown that low-intensity vibrations can speed up the healing process in a strain of diabetic mice commonly used to study delayed wound healing. The research team, led by Timothy Kohof the University of Illinois at Chicago, found that exposing the mice to barely perceptible vibrations five times a week for just 30 minutes promoted wound healing by increasing the formation of new blood vessels and of granulation tissue, a type of tissue critical in the early stages of healing. If researchers can show that the vibration technique also works in humans, this approach could one day offer a drug-free, non-invasive therapy for chronic wounds in people with diabetes.

This work also was funded by NIH’s National Institute of Dental and Craniofacial Research.

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