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

One study suggests that prostate tumors can spread by "spitting" a protein that "activates" dormant cancer cells.

Scientists have discovered that tiny fragments of a protein, called EN2, are absorbed by other cancer cells, causing them to change shape or to fuse.

It is believed that fused cancer cells are an aggressive sign of cancer that promotes the spread and survival of chemotherapy.

Resuming the EN2 standard also causes the cells to express a gene that helps to mask the tumors of the immune system, revealed the research "very important".

Scroll for the video

Researchers at the University of Bradford hope that the blockage of EN2 will lead to more effective cancer treatments.

The study was conducted on prostate tumors. Existing drugs for prostate cancer can cause erectile dysfunction or urinary incontinence.

Professor Richard Morgan, author of the study, said: "In order for tumors to survive, grow and spread, they must control the behavior of cancer cells and the normal cells that surround them and we have found a way to do it.

"The blockage of this process could be a potential target for future cancer treatment."

Prostate cancer is diagnosed every year in about 50,000 men in the UK, according to data from Cancer Research UK.

In the United States, approximately 174,650 men are diagnosed each year, according to statistics from the American Cancer Society.

EN2 has already been shown to play a role in the early development of the brain, while being present in large numbers in many types of cancers.

To determine the role it plays in prostate cancer, the researchers labeled the protein with a fluorescent green marker in the laboratory.

They then studied how it interacts with cancerous and normal cells in a human prostate model.

The results revealed that both cell types fuse with EN2-carrying vesicles and then absorb the protein.

To examine how this happens in more detail, the researchers performed an accelerated photograph, in which cells were taken every five minutes for 24 hours.

He showed that the cells ejected EN2, which was then absorbed by dormant cancer cells, activating, modifying, transforming or fusing together.

The cells then generate another vesicle containing EN2 that they can also expel.

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

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

Further analysis revealed that when normal cancer cells absorb EN2, they express a gene called MX2.

This generates an anti-viral response that can help tumors.

"We believe that cancer is trying to minimize the risk of infection of cells around it with a virus, to avoid any surveillance by the immune system," said Professor Morgan.

"This could hinder the effectiveness of immunotherapy treatments, which attempt to use viruses to kill cancer by stimulating the immune system for it to attack."

The researchers were surprised to find that the EN2 was expressed in the cell membrane rather than in its nucleus, which acts as a brain.

They think that it will give scientists more opportunities to block the action of EN2 by targeting a portion of the protein expressed on the surface of the cell.

The author of the study Hardev Pandha, a professor of medical oncology at the University of Surrey, added: Prostate cancer.

"The more we learn about prostate cancer, the more we can identify and treat this devastating disease."