TY - JOUR T1 - Modulation of Multidrug Resistance Gene Expression in Human Breast Cancer Cells by (-)-Gossypol-enriched Cottonseed Oil JF - Anticancer Research JO - Anticancer Res SP - 107 LP - 116 VL - 27 IS - 1A AU - WEIPING YE AU - HSIANG-LIN CHANG AU - LI-SHU WANG AU - YI-WEN HUANG AU - SHERRY SHU AU - MICHAEL K. DOWD AU - PETER J. WAN AU - YASURO SUGIMOTO AU - YOUNG C. LIN Y1 - 2007/01/01 UR - http://ar.iiarjournals.org/content/27/1A/107.abstract N2 - Background: Multidrug resistance (MDR) is a major impediment to successful cancer chemotherapy. P-glycoprotein (P-gp), the product of the multidrug resistance 1 (MDR1) gene, acts as an efflux pump and prevents sufficient intracellular accumulation of several anticancer agents, thus, playing a major role in MDR. Tamoxifen (Tam), ICI 182 780 (ICI) and Adriamycin (Adr) alone or with (-)-gossypol-enriched cottonseed oil [(-)-GPCSO] possible effects on cell growth inhibition and regulation of MDR1, mRNA and P-gp expression were examined in both an MDR human breast cancer cell line, MCF-7/Adr cells, and primary cultured human breast cancer epithelial cells (PCHBCEC). Materials and Methods: Cells were treated with 0.05% of (-)-GPCSO either in the absence or presence of either 0.1 μM Tam, ICI or Adr for 24 h. Results: Using the non-radioactive cell proliferation MTS assay, none of these chemotherapeutic agents alone inhibited MCF-7/Adr cell and PCHBCEC proliferation; meanwhile, the combination of 0.1 μM Tam, ICI or Adr with 0.05% (-)-GPCSO significantly reduced MCF-7/Adr cell growth by approximately 34%, 32% and 23%, respectively, of that of the vehicle-treated cells. For PCHBCEC, the combination of 0.05% (-)-GPCSO with 0.1 μM of Tam, ICI and Adr reduced cell growth to about 94%, 90%, and 71% respectively, of the vehicle treated PCHBCEC. Furthermore, (-)-GPCSO inhibited MDR1/P-gp expression in both MCF-7/Adr and PCHBCEC in a dose-dependent manner. Our results provide insight into the MDR-reversing potential of (-)-GPCSO in human breast cancer cells resistant to current chemotherapeutic agents. ER -