Increased Cell Membrane Fluidity May Improve Sensitivity to Ovarian Cancer Therapy

Increased Cell Membrane Fluidity May Improve Sensitivity to Ovarian Cancer Therapy
Cell membrane fluidity may determine ovarian cancer response to the anti-rheumatic drug Ridaura (auranofin) currently in trials for epithelial ovarian cancer, researchers found. The study, "Linking genotoxicity and cytotoxicity with membrane fluidity: A comparative study in ovarian cancer cell lines following exposure to auranofin," published in Mutation Research/Genetic Toxicity and Environmental Mutagenesis, shows that greater rigidity in the cell membrane prevents the cells from absorbing the drug and reduces its ability to kill the cancer. The anti-rheumatic drug Ridaura is currently under clinical trials in epithelial ovarian cancer (NCT01747798), which accounts for nearly 90 percent of all ovarian cancer cases. Ridaura works by inducing lethal DNA damage in BRCA1 mutated ovarian cancer cells. Cell membranes consist of lipid bilayers that surround the cells and control the substances that move into the inside or outside of the cells. Studies have reported that cells can increase the rigidity of their membranes (enriching them in cholesterol and sphingomyelin molecules) and impair intracellular drug uptake. To clarify how plasma membrane fluidity affects the responses of ovarian cancer to Ridaura, the research team led by Drs. Deepu Oommen and Nicholas Dodd, from the Genetic Toxicology & Ecotoxicology Research Group at Plymouth University, used two ovarian cancer cell lines — IGROV1 and OVCAR5. They used cutting edge technology to d
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