Mechanism identified that helps some cancers repair their DNA and survive: could be blocked with an old malaria drug

Scientists at the University of Copenhagen have pinpointed a crucial mechanism that enables certain cancer cells to repair DNA damage, a process vital for their survival and proliferation. The discovery, published in Science Signaling, centers on the gene NDRG1 and suggests a potential therapeutic target using an existing drug.

The research team, led by Garik Mkrtchyan, found that while normal cells also repair DNA damage, tumors often rely on enhanced repair systems to cope with the constant genetic errors generated by their rapid division and intense metabolism. If these damages were left unchecked, many cancer cells would perish. The study focused on identifying how tumors manage this self-inflicted damage.

Through computational analysis, genetic studies, and experiments on various tumor cell lines, the researchers identified NDRG1's significant role in the DNA damage response. Intriguingly, they found that quinacrine, an antimalarial drug with limited current use due to side effects, interferes with the interaction between NDRG1 and a protein called VCP. This disruption hinders the functioning of essential cellular repair mechanisms. By blocking this pathway, scientists hope to develop new treatments that exploit this specific vulnerability in cancer cells, potentially leading to more effective therapies.