Nuclear factor-ĸB plays a critical role in both intrinsic and acquired resistance against endocrine therapy in human breast cancer cells

摘要: Since more than 75% of breast cancers overexpress estrogen receptors (ER), endocrine therapy targeting ER has significantly improved the survival rate. Nonetheless, cancer still afflicts women worldwide and major problem behind it is resistance to therapy. We have previously shown involvement nuclear factor-κB (NF-κB) in neoplastic proliferation human cells; however, association with transformation ER-positive cells remains unclear. In current study, we focused on roles NF-κB hormone dependency by means MCF-7 cells. Blocking signals ER-negative stopped downregulation D-type cyclins. contrast, were resistant inhibition. Under estrogen-free conditions, levels reduced when compared original established cell subline exhibited tamoxifen resistance. Additionally, participated growth instead estrogen-ER axis consequently, interfering induced additive anticancer effects tamoxifen. MMP-9 production responsible for migration, as well expansion vivo, suppressed Therefore, suggest that a master switch both cancers.