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Study: Autophagy predicts which cancer cells live and die when faced with anti-cancer drugs
Date:1/10/2014

When a tumor is treated with an anti-cancer drug, some cells die and, unfortunately, some cells tend to live. A University of Colorado Cancer Center study published in the journal Nature Cell Biology details a possible difference between the susceptible and resistant cells: the rate at which cells are able to cleanse themselves via the process known as autophagy.

"In these studies, say we treat cells with the IC-50 of a drug - at that dose, 50 percent of cells should live and 50 percent of cells should die. But the fundamental question is why does cell A die whereas cell B lives? What we show is that the difference may be due to random variation in the amount of autophagy that's going on," says Andrew Thorburn, PhD, deputy director of the CU Cancer Center.

Previous studies show that autophagy promotes cell survival under conditions of stress or shortage, cells break down non-necessary components to provide energy or use the same strategy to prevent cellular damage by degrading and recycling potentially damaging proteins. And so it seems logical that cancer cells with low autophagy would have high mortality when faced with anti-cancer drugs. However, the current study shows that rates of cell death may increase or decrease depending on levels of autophagy and the specific mechanism of the anti-cancer drug.

"We separated cancer cells into populations with low and high autophagy and then treated them with two drugs, both of which should activate death. Interestingly, when treated with the first drug, cells with high autophagy had the highest mortality. But then when treated with the second drug, cells with low autophagy had the highest mortality. Depending on the drug, the effect of autophagy was opposite," Thorburn says.

Specifically, Thorburn and colleagues including first author Jacob Gump, PhD, treated high- and low-autophagy cell populations with chemicals TRAIL and Fas ligand, which activate cells' death receptor
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Contact: Garth Sundem
garth.sundem@ucdenver.edu
University of Colorado Denver
Source:Eurekalert

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