2023-08-30 07:20:32
An especially aggressive form of childhood cancer that forms in muscle tissue may have a new treatment option on the horizon.
Scientists have succeeded in inducing rhabdomyosarcoma cells to transform into normal, healthy muscle cells, a feat that might lead to the development of new treatments for the disease and might lead to similar discoveries for other types of human cancers.
“Cells literally turn into muscle,” says molecular biologist Christopher Vacock of Cold Spring Harbor Laboratory. “The tumor loses all the characteristics of cancer. It goes from a cell that just wants to make more of itself into a cell dedicated to shrinking. Because all of its energy and resources are now devoted to shrinkage, it doesn’t She can return to this breeding.”
Cancer arises when cells from different parts of the body mutate. Rhabdomyosarcoma is a type of cancer that appears most often in children and teens. It usually begins in skeletal muscles when cells in them mutate and begin to multiply and take over the body. They are also aggressive, and often fatal; Survival rates for the intermediate-risk group ranged between 50 and 70 percent.
One treatment option that appears promising is differential therapy. This was demonstrated when scientists noticed that leukemia cells were not fully mature, similar to undifferentiated stem cells that had not yet fully developed into a specific type of cell.
In previous work, Vacock and his team succeeded in reversing the mutation of cancer cells seen in Ewing’s sarcoma, another childhood cancer that usually appears in the bones.
The researchers wanted to see if they might replicate their success with rhabdomyosarcoma, which was thought to take decades for differentiation therapy.
They used a genetic screening technique to narrow down which genes might force rhabdomyosarcoma genes to continue developing into muscle cells. And they found the answer in a protein called nuclear transcription factor Y (NF-Y).
Rhabdomyosarcoma cells produce a protein called PAX3-FOXO1 that stimulates cancer proliferation, on which cancer depends.
The researchers found that inactivating NF-Y disrupts the activity of PAX3-FOXO1, which in turn forces the cells to continue their development and differentiate into mature muscle cells without any sign of cancerous activity.
The team says this is an essential step in developing differential therapy for rhabdomyosarcoma, and might speed up the expected timeline for such treatments.
The research was published in the Proceedings of the National Academy of Sciences.
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