Alyssa A Sprouse1, Brittney-Shea Herbert2. 1. Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, U.S.A. 2. Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, U.S.A. Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, U.S.A. Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, IN, U.S.A. Indiana Institute for Personalized Medicine, Indianapolis, IN, U.S.A. brherber@iu.edu.
Abstract
BACKGROUND: Resveratrol (RES) inhibits cell growth, induces apoptosis and augments chemotherapeutics in multiple cancer types, although its effects on drug-resistant cancer cells are unknown. MATERIALS AND METHODS: To study the effects of resveratrol in triple-negative breast cancer cells that are resistant to the common cancer drug, paclitaxel, a novel paclitaxel-resistant cell line was generated from the MDA-MB-231 cell line. RESULTS: The resistant MDA-MB-231/PacR cells exhibited a 12-fold increased resistance to paclitaxel. RES treatment reduced cell proliferation and colony formation and increased senescence and apoptosis in both parental and resistant cells. Importantly, RES augmented the effects of paclitaxel in both cell lines. Up-regulation of the MDR1 and CYP2C8 genes were shown to be potential mechanisms of paclitaxel resistance in the resistant cells. CONCLUSION: RES, both alone and in combination with paclitaxel, may be useful in the treatment of paclitaxel-sensitive and paclitaxel-resistant triple-negative breast cancer cells. Copyright
BACKGROUND:Resveratrol (RES) inhibits cell growth, induces apoptosis and augments chemotherapeutics in multiple cancer types, although its effects on drug-resistant cancer cells are unknown. MATERIALS AND METHODS: To study the effects of resveratrol in triple-negative breast cancer cells that are resistant to the common cancer drug, paclitaxel, a novel paclitaxel-resistant cell line was generated from the MDA-MB-231 cell line. RESULTS: The resistant MDA-MB-231/PacR cells exhibited a 12-fold increased resistance to paclitaxel. RES treatment reduced cell proliferation and colony formation and increased senescence and apoptosis in both parental and resistant cells. Importantly, RES augmented the effects of paclitaxel in both cell lines. Up-regulation of the MDR1 and CYP2C8 genes were shown to be potential mechanisms of paclitaxel resistance in the resistant cells. CONCLUSION:RES, both alone and in combination with paclitaxel, may be useful in the treatment of paclitaxel-sensitive and paclitaxel-resistant triple-negative breast cancer cells. Copyright
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