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. 2014 Nov 25;112(2):345–351. doi: 10.1038/bjc.2014.595

Figure 1.

Figure 1

FOXA1 knockdown boosts the efficacy of paclitaxel only in ER-positive breast cancer cells. MCF-7, T-47D, and SK-BR-3 cells were treated with paclitaxel for 96 h after knockdown of FOXA1 by siRNA. (A) Proliferation assay revealed that FOXA1 suppression enhances responses to chemotherapy in MCF-7 and T-47D, both hormone-positive cell lines. This trend was not observed in hormone-negative SK-BR-3 cells. (B) Western blot showed that FOXA1 suppression induces MCF-7 cells to express more CK5/6, indicating that these cells have an increased basal propensity. However, this phenomenon was not seen in T-47D. Vimentin is not shown here since none of the three cell lines expressed this protein. (C) The effects of FOXA1 knockdown were also seen in paclitaxel-resistant MCF-7-PTXR cells, suggesting that resistance to chemotherapy had been overcome. *P<0.05, **P<0.01.