Melanoma cells use ‘molecular drills’ to invade new tissues, research finds

pharmafile | August 8, 2022 | News story | Sales and Marketing  

Scientists have identified a nerve cell gene that enables melanoma cells to branch out and invade new tissues. Research from the Institute of Cancer Research (ICR) has found that the gene allows cancer cells to create molecular drills, which break through surrounding tissues, enabling spread.

Melanoma skin cancer cells harness a gene usually used by growing nerves to escape from their immediate area, and spread through tissues, the scientists found.

Blocking the gene, the ICR has shared, could open a new avenue for developing treatments that prevent metastasis (the spread of cancer cells from the place they originated, to other parts of the body).

Researchers found that melanoma cells utilise the ARHGEF9, to create ‘molecular drills’ which help them attach to and penetrate through surround cells and structures. These drills are also called filopodia, and are involved in the growth and development of new nerves.

Professor Chris Bakal, Professor of Cancer Morphodynamics at The Institute of Cancer Research, London, commented: “Our work shows that melanoma cells borrow use of ARHGEF9 from nerve cells to change shape, branch out and invade new tissues. It’s incredibly important that we understand how cancer cells change their shape to become more aggressive and invasive. When cancers metastasise, they become much harder to treat.”

Scientists from the ICR, London, grew cells in bioengineered 3D cell matrix and depleted hundreds of genes at a time. Using robotic microscopy, and sophisticated image analysis, they identified which genes were important for cancer cell shape.

Meanwhile, depleting ARHGEF9 destabilised the molecular drills on the melanoma cells, and additionally lessened these cells’ ability to change shape.

“We’re working to better understand how cancer cells change shape and invade new tissues, so that one day we can find treatments that stop it,” Continued Professor Bakal. “Our next step will be to look at the broader impacts of blocking ARHGEF9 to explore whether it could be suitable to target it with a drug to stop the gene from helping the cancer to spread.”

Professor Clare Isacke, Dean of Academic and Research Affairs, at The Institute of Cancer Research, London, concluded: “Although it is early research, and more work needs to be done, by understanding more about how skin cancer spreads, we could open up new avenues for developing treatments which stop cancer in its tracks.”

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