NSAIDs Induce Anti-Cancer Gene Code

Researchers have uncovered a mechanism that helps to explain the cancer-preventing action of nonsteroidal anti-inflammatory drugs (NSAIDs).

Investigators at Harvard University (Boston, MA, USA) worked with both cancer cells growing in tissue culture and a mouse model of human prostate cancer. Their purpose was to explain findings showing that NSAIDs protect against cancer by a pathway not related to the inhibition of cyclooxygenase (COX).

Results published in the December 15, 2006, issue of Cancer Research revealed that induction of the gene MDA-7/IL-24 (melanoma differentiation associated gene-7/interleukin-24) by several NSAIDs was an essential step for induction of apoptosis and G2-M growth arrest in cancer cells in culture and inhibition of tumor growth in animals. The effect of MDA-7/IL-24 was linked to its ability to activate two growth arrest DNA damage genes: GADD45-alpha and GADD45-gamma.

"Current clinical trials are evaluating a range of NSAIDs for a variety of cancers without any clear vision of the best way to use them,” said senior author Dr. Towia Libermann, associate professor of medicine at Harvard Medical School. "The fact that upregulation of this single gene--MDA-7/IL-24--correlated not only with cell death induction of numerous types of cancer but also among various diverse classes of NSAIDs, makes this discovery particularly exciting. The level of MDA-7/IL-24 gene expression in cancer patients may emerge as a new biomarker for monitoring patients' responses to certain therapies, and may help determine whether drugs such as NSAIDs are hitting their intended targets.”



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