Chronic inflammation is a significant contributor to cancer development globally. A recent study published in Nature Communications sheds light on how the drug pitavastatin can effectively prevent cancer development in cases of chronic inflammation by blocking interleukin 33 (IL-33) expression.

The research conducted by Jong Ho Park and colleagues reveals that IL-33 plays a crucial role in initiating cancer-prone chronic inflammation. The study uncovers that environmental triggers activate the Toll-like receptor (TLR)3/4-TBK1-IRF3 pathway, leading to the induction of IL-33 in the skin and pancreas, which are common sites of inflammation.

Through a screening of an FDA-approved drug library, pitavastatin was identified as a potent inhibitor of IL-33 expression. The drug achieves this by blocking the recruitment and activation of TBK1 through the mevalonate pathway inhibition. Consequently, pitavastatin demonstrates the ability to prevent chronic pancreatitis and its associated cancer development in a manner dependent on IL-33.

The study further highlights the high activity of the IRF3-IL-33 axis in cases of chronic pancreatitis and pancreatic cancer in humans. Interestingly, the use of pitavastatin is linked to a significant reduction in the risk of chronic pancreatitis and pancreatic cancer among patients.

These findings underscore the significance of inhibiting the TBK1-IRF3-IL-33 signaling axis in suppressing cancer-prone chronic inflammation. The research suggests that statins, such as pitavastatin, present a safe and effective strategy for prophylaxis against chronic inflammation and its cancer-related consequences.

As the prevalence of cancer-prone chronic inflammation continues to rise globally, the study emphasizes the importance of developing improved strategies for cancer prevention in high-risk populations. Chronic pancreatitis, inflammatory bowel disease, and hepatitis are among the conditions associated with an increased risk of cancer, making the need for effective prevention strategies more urgent than ever.