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Fig. 3 | Breast Cancer Research

Fig. 3

From: SNAI2 upregulation is associated with an aggressive phenotype in fulvestrant-resistant breast cancer cells and is an indicator of poor response to endocrine therapy in estrogen receptor-positive metastatic breast cancer

Fig. 3

Inhibition of SNAI2 induces epithelial characteristics and impairs growth of fulvestrant-resistant breast cancer cell lines. a MCF-7-based fulvestrant-resistant and parental sensitive cells were transfected with small interfering RNA (siRNA) against SNAI2 leading to a reduction at the messenger RNA (mRNA) level, as evaluated by reverse transcription (RT)-quantitative (q)PCR (RT-qPCR). SNAI2 knockdown resulted in a significant reduction in the migration ability of both fulvestrant-resistant and fuvestrant-sensitive cells, as depicted in b representative micrographs (purple-stained cells, × 20 magnification) and c by column diagram analysis of the percentage of cells that migrated following SNAI2 knockdown. d E-cadherin mRNA expression after SNAI2 silencing determined by RT-qPCR. Gene expression was normalized using PUM1. e Effect of SNAI2 knockdown on growth of fulvestrant-resistant and parental sensitive cells, as measured by crystal violet-based colorimetric assay. f Cell growth of fulvestrant-resistant and parental sensitive cells following treatment with the selective p53-SNAIL binding inhibitor (GN25), fulvestrant, the two drugs in combination or vehicle (control), as measured by crystal violet-based colorimetric assay: *p < 0.05. Data are shown with error bars representing mean ± standard deviation. g Immunocytochemical analysis of SOX2 protein in formalin-fixed paraffin-embedded fulvestrant-resistant and fulvestrant-sensitive cells (× 20 magnification). h Protein expression levels of SOX2 following SNAI2 knockdown determined by western blotting. β-actin was used as loading control. A representative of three independent experiments is shown

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