Scientists from Case Western Reserve University's School of Medicine have discovered a potential treatment that may steer cancer cells toward their own destruction. The study focused on a particular gene that was found to influence levels of a tumor-fighting protein called 53BP1, the heightened presence of which makes cancer cells more vulnerable to existing forms of treatment.

The proposed therapeutic approach centers on the repairing of DNA, a process that sees the body mend molecules damaged by everything from reactive oxygen components to radiation and chemical agents. More specifically, it focuses on a double-strand break, a type of injury that sees both strands of the double helix severed, leading to damaged and dead cells.

One mechanism that the body uses to fix these double-strand breaks is gluing the DNA strands together again, but this isn't ideal as it renders those strands less effective in sending information through to the cell, meaning the cells are often left to die anyway. Another method of repair used by the body is using information from undamaged DNA to mend the broken DNA, a more effective way of repairing the broken double strands.

Through their study, the researchers observed the functions of an important gene in this process called UbcH7, known to help regulate the repair of broken double strands. What they found was that depleting levels of UbcH7 resulted in a significant boosting of the tumor-suppressing 53BP1 protein, which in turn drives the cancer cells toward the first, less effective path of repair: the gluing method. The team says the approach could complement current forms of treatment.

"What we propose is increasing the level of 53BP1 to force cancer cells into the error-prone pathway where they will die," says Youwei Zhang, assistant professor of pharmacology at the university's School of Medicine. "The idea is to suppress deliberately the second accurate repair pathway where cancer cells would prefer to go. It is a strategy that would lead to enhanced effectiveness of cancer therapy drugs.”

The team's findings so far are the product of laboratory experiments, but the promising results has them planning on testing the approach in animal models. This would involve introducing the 53BP1 protein in mice and then treating them with radiation therapy and chemotherapy drugs.

The research findings were published in the journal Proceedings of the National Academy of Sciences.