The functioning of an important gene protecting cells from cancer is discovered by a Catalan-American study

Barcelona (ACN).- Catalan researchers, together with American scientists, have discovered how the P53 Tumour Suppressor Gene regulates itself, a gene that prevents healthy cells from turning into tumour cells. 50% of tumours are related to mutations of this gene, according to the researchers. The study has been developed by the Bellvitge Institute of Biomedical Research (IBIDELL), based in Greater Barcelona, and the University of Cincinnati. It was led by George Thomas. Researchers have discovered the role of the noncoding 5S rRNA molecule, which regulates the P53 Tumour Suppressor Gene. When the cell functions correctly, the levels of P53 are low and stable, but when something wrong is detected, the levels increase and cause the cell’s death. This mechanism avoids the damaged cells growing in a chaotic way and developing a tumour. George Thomas explained that understanding how the P53 works and regulates itself is extremely important since “more than half of the tumours present mutations of this gene”. Thomas announced that currently they are working towards developing a clinical essay to test this control mechanism.

The cellular ribosomes are the structure in charge of forming proteins. When in this process something goes wrong, cells might be damaged and this is when conditions such as cancer can happen. Researchers at the IBIDELL’s Metabolism and Cancer Group and the University of Cincinnati have discovered how one of the main cellular control mechanisms works to prevent damaged cells surviving, growing and forming a tumour.

Hdm2 is the main protein that in normal conditions is in charge of keeping the P53 levels low. Researchers have discovered exactly how the 5S rRNA molecule works, which is one of the main elements influencing the protein Hdm2 and therefore the P53 gene. When ribosomes are damaged, cells can get damaged and, the 5S rRNA molecule deviates from its regular route and unites with the Hdm2 protein, blocking the latter’s activity. Since the Hdm2 protein then does not work any longer to keep the P53 levels low, these levels increase and cause the cell’s death. Since the damaged cell dies, there is no risk it forms a tumour.