Health
A new mechanism of DNA damage is elucidated
A team of researchers at the University of California (UC) Irvine has uncovered a previously unknown mechanism by which damaged cells' DNA triggers an inflammatory immune response. This discovery provides new understanding of a new type of cell signaling that could lead to more effective treatments for cancer.
This research Structural biology and molecular biology of nature In an article titled “ATM and IRAK1 coordinate two distinct mechanisms of NF-κB activation in response to DNA damage”
Researchers have discovered that when cells are too damaged to repair properly, ultraviolet radiation or certain chemotherapy drugs activate certain responses that prevent cells from becoming cancerous.
“Cellular DNA damage induces the expression of inflammatory genes,” the researchers wrote. “However, the mechanisms by which cells mount an innate immune response in the presence of DNA damage that blocks transcription remain unclear. Here we show that genotoxic stress induces acute activation of the transcription factor NF-κB through two distinct pathways. We found that each is caused by a different type of DNA damage and regulated by either the ataxia telangiectasia mutated (ATM) kinase or the IRAK1 kinase.
“This discovery could have important implications for cancer treatment,” explained corresponding author Rémi Buisson, Ph.D., associate professor of biochemistry at the University of California, Irvine. “Understanding how different cancer cells respond to DNA damage could lead to more tailored and effective treatments, reduce negative side effects, and improve patients' quality of life. there is.”
Scientists have long understood that when both DNA strands are broken, the ATM enzyme causes activation of the protein NF-κB within the cell, leading to the generation of inflammatory signals. In this study, led by postdoctoral fellow Dr. Elodie Brunique and supported by graduate student Ambrosio Sánchez, DNA damage caused by UV exposure or treatment with chemotherapeutic drugs such as actinomycin D and camptothecin inhibits the IRAK1 enzyme. It has been shown to induce NF. -κB sends signals that recruit immune cells.
Researchers have developed an imaging technique to analyze how NF-κB is regulated at the cellular level. They were able to measure cellular responses to damaged DNA at the single-cell level and observed a new pathway to NF-κB activation. They found that cells release IL-1α protein after certain types of injury. It does not act on the cell itself, but moves to neighboring cells, where it induces the IRAK1 protein and subsequently initiates the NF-κB inflammatory response.
“Our findings will help us better understand the effects of certain types of chemotherapy drugs used to treat patients and cause DNA damage. and IRAK1 proteins vary widely in different cancer cell types, suggesting that not all patients will respond to treatment in the same way, Bouisson said. said. “By proactively assessing these protein levels, physicians may be able to customize treatments to individual patient needs and improve success rates.”
In the future, the researchers plan to continue their work by testing their findings in mouse models that lack specific factors involved in the new pathway.
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