Two fatal hits can lead to cell death after defective division, thus preventing the risk of tumors. This discovery is the result of research conducted by the University of Trento and the Research Center for Molecular Medicine of the Austrian Academy of Sciences, published in the journal Science Advances.
The research group, led by Andreas Villunger of CeMM Vienna and Luca Fava of the University of Trento, identified that an excessive number of centrosomes (protein structures that separate chromosomes) signals a defective cell division (mitosis). This is interpreted as an alarm signal that activates a protein complex known as PIDDosoma.
“This alarm bell activates the enzyme caspase-2, triggering two mechanisms that lead to cell death,” says Villunger.
In the first mechanism, the protein BID leads the cell to suicide, destroying the mitochondria, the cell’s power plants. The second mechanism involves the famous tumor suppressor p53, which activates additional signaling pathways to induce cell death. This “double hit” ensures the elimination of cells with multiple centrosomes, even if one of the two proteins, BID or p53, is absent or inhibited.
This discovery could have important therapeutic implications, especially in the fight against blood tumors. By enhancing the destructive effect of the PIDDosoma, it could improve the effectiveness of therapies designed to sabotage the cell division of diseased cells. Villunger points out that “analyzing BID and caspase-2 activity in tumor cells could potentially identify patients most likely to respond to drugs that interfere with cell division.” These findings offer new insights into the personalization of cancer therapies and may help develop more effective treatments for patients.
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