Prostate cancer cells release a protein that promotes self-growth


Recently, a study called 'Membrane insertion and secretion of Engrailed-2 (EN2) transcription factor by prostate cancer cells may induce antiviral activity in the stroma' has been published in the Scientific Reports. The study, led by researchers at the University of Bradford and the University of Surrey, describes that prostate cancer cells nucleus "spit out" a protein, which was absorbed by other cells around them, including normal cells, triggering changes that promote tumors growth and help cancer cells escape from the attack of the human immune system.  

In order to survive, grow and spread, tumors need to control the behavior of cancer cells and surrounding normal cells. So stopping this process may become a potential target for future cancer treatment.

Previous studies have demonstrated that EN2 in urine is a powerful diagnostic biomarker for prostate cancer. On this basis, the researchers mainly studied the protein EN2, which plays a role in the early development of the brain, but is also highly expressed in many cancer cells.

The team labeled the EN2 protein with a green fluorescent label and then studied the activity of the green fluorescent protein in human prostate cancer cells, normal prostate cells and bladder cancer, melanoma and leukemia cells. They found that both cancer and normal cells took up proteins from other cells.

They also took time-lapse photography of prostate cancer cells, taking pictures every 5 minutes for 24 hours. The video shows that the cells eject a small portion of the green fluorescent protein that is then taken up by other dormant cancer cells, causing them to reactivate, change shape or fuse together.

The fusion of cancer cells is relatively uncommon and is associated with highly aggressive cancers. Because fusion may result in new and unpredictable hybrid cells, these cells are more proliferative and resistant to chemotherapy and radiation.

Molecular analysis of normal prostate cells showed that absorption of EN2 caused them to express a gene called MX2, which stimulates an antiviral response. Therefore, cancer may minimize the chance of infection of the surrounding cells as soon as possible through this way, thus avoiding the identification of the immune system. This also undermines the low effectiveness of using viruses to treat cancer in immunotherapy.

The researchers also found that EN2 proteins in cell membranes and nucleus are very rare. And then they recognized that the portion of the protein available on the cell surface is a potential therapeutic target for prostate cancer.

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