By a News Reporter-Staff News Editor at Drug Week -- Researchers from the University of Alberta are abuzz after using fruit flies to find new ways of taking advantage of caffeine's lethal effects on cancer cells-results that could one day be used to advance cancer therapies for people (see also DNA Research).
Previous research has established that caffeine interferes with processes in cancer cells that control DNA repair, a finding that has generated interest in using the stimulant as a chemotherapy treatment. But given the toxic nature of caffeine at high doses, researchers from the U of A instead opted to use it to identify genes and pathways responsible for DNA repair.
"The problem in using caffeine directly is that the levels you would need to completely inhibit the pathway involved in this DNA repair process would kill you," said Shelagh Campbell, co-principal investigator. "We've come at it from a different angle to find ways to take advantage of this caffeine sensitivity."
The research team found that fruit flies with a mutant gene called melanoma antigen gene, or MAGE, appeared normal when fed a regular diet but died when fed food supplemented with caffeine. On closer inspection, they found the mutant flies' cells were super-sensitive to caffeine, with the drug triggering "cell suicide" called apoptosis.
Through this work, researchers identified three genes responsible for a multi-protein complex, called SMC5/SMC6/MAGE, which regulates DNA repair and the control of cell division. Neither process works properly in cancer cells.
This finding is significant because it means that scientists one day could be able to take advantage of cancer-cell sensitivity to caffeine by developing targeted treatments for cancers with specific genetic changes.
The study was led by Rachel Wevrick and Shelagh Campbell, who published their results in the March issue of the peer-reviewed journal PLOS One.
Keywords for this news article include: Cancer, Caffeine, Genetics, Oncology, DNA Repair, Proteomics, DNA Research, Anorexigenic Agent, Deoxyribonucleic Acid, University of Alberta, Phosphodiesterase Inhibitors, Central Nervous System Stimulants.
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