AI Article Synopsis
- Persistent inflammation is increasingly recognized as a significant contributor to cancer development, with evidence from both preclinical and clinical studies.
- Cyclooxygenase-2 (COX-2) is an important enzyme linked to inflammation that is often overexpressed in colorectal cancer and other cancers, particularly when inflammation does not resolve.
- The review discusses COX-2's complex role, including both its pro-inflammatory activities and its ability to produce anti-inflammatory substances, which may explain the adverse effects of long-term COX-2 inhibitors used in cancer prevention trials.
Article Abstract
Mounting evidence from preclinical and clinical studies suggests that persistent inflammation functions as a driving force in the journey to cancer. Cyclooxygenase-2 (COX-2) is a key enzyme involved in inflammatory signaling. While being transiently upregulated upon inflammatory stimuli, COX-2 has been found to be consistently overexpressed in human colorectal cancer and several other malignancies. The association between chronic inflammation and cancer has been revisited: cancer can arise when inflammation fails to resolve. Besides its proinflammatory functions, COX-2 also catalyzes the production of pro-resolving as well as anti-inflammatory metabolites from polyunsaturated fatty acids. This may account for the side effects caused by long term use of some COX-2 inhibitory drugs during the cancer chemopreventive trials. This review summarizes the latest findings highlighting the dual functions of COX-2 in the context of its implications in the development, maintenance, and progression of cancer.
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| http://dx.doi.org/10.1016/j.bcp.2024.116259 | DOI Listing |
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