Targeting GLI1 expression in human inflammatory breast cancer cells enhances apoptosis and attenuates migration.

摘要: Inflammatory breast cancer (IBC) is an aggressive subtype of with distinct molecular profiles. Gene expression profiling previously identified sonic hedgehog (SHH) as part a gene signature that differentially regulated in IBC patients. The effects reducing GLI1 levels on protein expression, cell proliferation, apoptosis and migration were determined by immunoblots, MTT assay, Annexin-V/PI assay conventional automated assays. Evaluation panel lines revealed elevated typically marker for hedgehog-pathway activation, triple-negative, highly invasive line, SUM149 its isogenic-derived counterpart rSUM149 has acquired resistance to ErbB1/2 targeting strategies. Downregulation small interfering RNA or molecule inhibitor resulted decreased proliferation increased apoptosis. Further, suppression these significantly inhibited assessed wound-healing compared MCF-7, non-invasive line low expression. A novel high-content allowed us quantify multiple silencing including significant decreases distance travelled linearity movement. Our data reveal role survival migration, which supports the feasibility therapeutic strategy