An international research group coordinated by the Molecular Biotechnology Center of the University of Turin has identified a key mechanism in cellular aging processes. The research results were published in Science.
“Starting from the study of tumors, we made an unexpected discovery”, explains the coordinator of the study Emilio Hirsch, professor at the University of Turin, to ANSA. “The cells replicate with a very complex process that leads to the last step, in which the single cell is ‘cut’ into two independent cells. This last step is called cytokinesis. ‘expression of the PIK3C2A and VPS36 genes, cause this cut not to occur correctly. When this occurs, the cell implements the cellular senescence program, which leads to aging first of the cell and then of the whole organism “.
The team arrived at this discovery by studying a rare genetic condition in which children born with a genetic deficiency of PI3K-C2alpha (the protein expressed by the PIK3C2A gene) show signs of premature aging, including infant cataracts. “Cataracts are an expression of the aging of the lens cells,” says Hirsch.
“In the crystalline the process that we have identified is particularly evident because, for reasons we do not yet know, the cells do not have mechanisms capable of compensating for the defects of the PIK3C2A gene. So when the availability of the protein is scarce, for genetic or because it fades as a consequence of aging, cataracts develop “.
The research represents the development of previous works in the oncology field: “Uncontrolled cell proliferation is the basis of cancer. And in this process the PIK3C2A gene and the enzyme it expresses play an important role”, explains the researcher who is studying the link. between PIK3C2A and breast cancer aggression with a contribution from the AIRC Foundation. (HANDLE).
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