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Researchers from the University of California, Irvine have uncovered a previously unidentified mechanism causing an inflammatory immunological response in cells upon DNA damage. This finding reveals a new type of cell signaling that might result in more successful cancer treatments.
Published online today in the journal Nature Structural & Molecular Biology, the study revealed that UV irradiation or some chemotherapy medications stimulate a particular response when cells are too damaged to be rebuilt correctly, therefore preventing them from becoming malignant.
Knowing how various cancer cells respond to DNA damage could help produce more customized and powerful treatments, therefore lowering undesirable side effects and perhaps enhancing patient quality of life.
Scientists have long known that the ATM enzyme activates the protein NF-κB inside the cell when both DNA strands break, therefore producing inflammatory signals.
This investigation demonstrated that the IRAK1 enzyme promotes the recruitment of immune cells by inducing NF-κB to transmit signals when DNA damage occurs as a result of UV exposure or chemotherapeutic drug treatment.
The research team created a sophisticated imaging method to examine cellular level regulation of NF-κB. At the single-cell level, the researchers were able to exactly track a cell’s reaction to damaged DNA and found an entirely new means to NF-κB activation. After particular kinds of injury, they discovered that cells produce the IL-1α protein. It moves to surrounding cells, where it activates the IRAK1 protein, therefore starting the NF-κB inflammatory response rather than acting on the cell itself.
The results will provide a better knowledge of the effects of several forms of chemotherapy medications applied to patients and resulting in DNA damage. The researchers found that variations in cancer cell types greatly affect the immune process-related IL-1α and IRAK1 proteins. This implies that different patients will respond differently to treatment.
Through pre-evaluation of these protein levels, physicians may be able to customize treatments catered to the needs of certain patients for higher success rates.
The scientists will keep working by verifying their results on mice models lacking of particular components engaged in the new pathway.
Sources:
Elodie Bournique et al. (2025). ATM and IRAK1 orchestrate two distinct mechanisms of NF-κB activation in response to DNA damage, Nature Structural & Molecular Biology. DOI: 10.1038/s41594-024-01417-0
https://phys.org/news/2025-01-newly-mechanism-triggers-immune-response.html
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