Prostate tumors spread by "spitting" a protein that wakes dormant cancer cells

Window on the World – A new study found that cancer cells in the prostate changed the behavior of other surrounding cells, including normal cells, by "spitting" proteins into their nucleus.

The small pieces of protein, called EN2, are absorbed by other cells, resulting in changes that promote tumor growth and fusion, helping to hide cancer from the immune system.

The process was first documented on video by researchers from the University of Bradford and the University of Surrey.

Researchers say this is "very important" because the cancerous cells in fusion are associated with a "more aggressive" disease, more common and resistant to chemotherapy.

The study concluded that taking "EN2" brings cells to gene expression that hides tumors of the immune system.

The new study was conducted by the University of Bradford, led by Professor Richard Morgan, director of the Cancer Institute.

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To determine the role of this protein in prostate cancer, the researchers placed a green marker in the laboratory and then studied its interaction with all the cancer cells and normal cells of a human prostate model.

The results revealed that both cell types combine with "EN2" vesicles and then absorb the protein.

To see how this happened in more detail, the researchers photographed intervals, where cells were taken every five minutes for 24 hours.

The video reveals that the cells release the "EN2" protein, which is then "eaten" by dormant cancer cells, which activate or modify the form or fuse together. The cells then create another vial containing "EN2" that can also be expelled.

"We think it's important because cell fusion in cancer is relatively unusual and associated with a very aggressive disease," said Professor Morgan.

This can lead to unpredictable new hybrid cells that often spread better at different sites and survive despite chemotherapy and radiation therapy. "

The molecular analysis of natural prostate cells also showed that the consumption of "EN2" caused the expression of a gene called "MX2" that generated an antiviral response.

The researchers were surprised to find "EN2" in the cell membrane instead of the nuclei, which is unusual for this type of protein. Therefore, they think this will give them a greater chance of preventing the work of "EN2" by targeting a portion of the protein that is expressed on the surface of the cell.

Source: Daily Mail