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Mechanism through which cyclooxygenase-2 enzymes promote development of colon cancer is discovered

The molecular interactions that allow cyclooxygenase-2 enzymes to promote development of colon cancer have been discovered, according to an article published online on June 30th by the Proceedings of the National Academy of Sciences.

In laboratory studies involving human and rat cells, the investigators defined the multiple steps initiated by the family of enzymes, including prominent roles for cyclic adenosine monophosphate and proteins called inhibitors of apoptosis. The result of the molecular interactions is suppression of apoptosis, resulting in uncontrolled cell growth and eventually colon cancer.

Specifically, apoptosis is a result of balanced molecular actions taking place at 2 different starting points. An extrinsic pathway, also called the death receptor pathway, activates 1 set of molecules. A second, intrinsic pathway is mediated by mitochondria. As the 2 pathways meet and join they cause chemical reactions down a final pathway that result in cell death. The proteins termed inhibitors of apoptosis act at the point where the 2 pathways merge.

The chain of events begins with enzyme-induced increases in formation of prostaglandins, and prostaglandin-induced increases in formation of cyclic adenosine monophosphate. Cyclic adenosine monophosphate is the molecule that actually blocks normal cell death through activation of inhibitors of apoptosis.

According to Paul Insel, MD, senior author of the study, the findings may have implications for understanding the origins of other cancers in which cyclooxygenase-2 or similar enzyme activity appear to play a role, including certain lung cancers, prostate cancer, squamous cell carcinomas of the head and neck, and some types of breast cancer.

In addition, by pinpointing each step in the molecular chain of events initiated by cyclooxygenase-2 enzymes, the study offers potential new targets for drug therapies that have greater effectiveness and fewer side effects than those associated with nonsteroidal anti-inflammatory agents. Long-term use of these agents is associated with a 40 to 50 percent decrease in the incidence of colon cancers.

 


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