How a common diabetes drug could slow cancer and aging studied
The diabetes drug metformin has a unique molecular mechanism that researchers say could slow aging and even the progression of cancer in ways that have nothing in common with its antidiabetic properties.
University of Montreal scientists uncovered the drug’s potential when they discovered the antidiabetic drug stops inflammatory cytokines that from being produced as part of the body’s immune defense.
Cytokines are important for fighting disease but when production of the molecules becomes chronic it can cause cellular aging. An example is the type of chronic inflammation that comes from smoking.
Dr. Gerardo Ferbeyre, senior author and a University of Montreal biochemistry professor said in a press release, “We were surprised by our finding that metformin could prevent the production of inflammatory cytokines by old cells” that he adds are especially proficient at making and releasing cytokines.
Michael Pollack of the Segal Cancer Centre of the Jewish General Hospital, McGill University, Dr. Ferbeyre and his team discovered that metformin works directly at the level of the regulation of cytokine genes in a way that is completely unrelated to the drug’s antidiabetic effect.
“The genes that code for cytokines are normal, but a protein that normally triggers their activation called NF-B can’t reach them in the cell nucleus in metformin treated cells”, Dr. Ferbeyre explained.
Lead authors of the study Olga Moiseeva and Xavier Deschênes-Simard. Dr. Ferbeyre emphasize the importance of the study for understanding how the body defends itself from cancer.
Metformin is inexpensive, relatively safe and could provide a new treatment for slowing aging and the progression of some cancers, the authors note.
Dr. Ferbeyre says the next step is “…determining the specific targets of metformin” to tap into the diabetes drug’s beneficial effects. The common diabetes drug inhibits chronic inflammation that could help slow aging and lead to improved cancer survival.
“Metformin inhibits the senescence-associated secretory phenotype by interfering with IKK/NF-B activation”
Olga Moiseeva et al.
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