to begin examining whether routine use of anti-inflammatory agents had any effect on a person’s risk of developing several types of cancer, including colorectal cancer, breast cancer and ovarian cancer.
“Since then, studies have indeed shown that at clinically relevant concentrations, NSAIDs may be effective in the prevention and treatment of common cancers,” he says. These anti-cancer effects have been attributed, in large part, to NSAIDs’ potential to induce cell death, which appears to stem from the drugs’ inhibition of the COX (cyclooxygenase) enzymes, the primary mechanism by which NSAIDs guard against pain.
“However,” adds Libermann, “COX inhibition did not appear to be the only anti-cancer pathway being targeted by the compounds. We, therefore, undertook a comprehensive review of NSAIDs in order to decipher the precise molecular mechanisms that were at work.”
Using whole genome microarray analysis, Libermann and first author Luiz Zerbini, PhD, a researcher in the BIDMC Genomics Center and Instructor of Medicine at HMS, examined more than 20,000 genes to identify potential mechanisms for cell death induction.
“When we analyzed the genes that were upregulated by NSAIDS, one in particular stood out from the rest,” says Zerbini. “And that was MDA-7/IL-24.”
A cancer specific cytokine, MDA-7/IL-24 was already familiar to the investigators as a novel tumor suppressor gene, says Libermann. “Viral delivery of MDA-7/IL-24 is currently being evaluated in several clinical trials as a therapeutic agent against various cancers, and enhanced levels of the gene have also been correlated with prolonged survival in patients with non-small lung cancer.”
Following their identification of this cytokine, the investigators used an interfering RNA approach to block MDA-7/IL-24 gene expression in cancer cells, thereby demonstrating the necessity of NSAID-mediated induction of the gene to destroy cancer cells. They also used a mouse mPage: 1 2 3 4 Related medicine news :1
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