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. 2017 Aug 2;8(39):66033–66050. doi: 10.18632/oncotarget.19789

Figure 2. Effects of 7-ketocholesterol (7-KC), 27-hydroxycholesterol (27-HC), and fulvestrant on P-glycoprotein function in breast cancer cell lines.

Figure 2

P-glycoprotein function was monitored by verapamil inhibited efflux of rhodamine (Rh)123 (A) and cellular accumulation of doxorubicin (B and C). Panel (A) shows the alterations of Rh123 efflux affected by 48-h exposure to 7-KC in cells cultured in 2% and 10% fetal-bovine-serum (FBS)-supplemented media. Rh123 efflux was determined as described in the Methods. Panel (B) shows the influence of the estrogen receptor (ER) antagonist fulvestrant on 7-KC-reduced doxorubicin accumulation in cells cultured in 2% FBS-supplemented medium. Cells were exposed to 5 μM fulvestrant together with 7-KC for 48 h and then doxorubicin accumulation was determined as described in the Methods. The results are presented as means ± SD of three independent experiments. To prevent the interference of trace E2 level in FBS-supplemented medium, MCF-7 or T-47D cells were exposed to estradiol (E2), 7-KC and 27-hydroxycholesterol (27-HC) in charcoal/dextran-stripped FBS (DCCFBS)-supplemented medium and doxorubicin accumulation were determined (C). Data are presented as means ± SD of three independent experiments. *p < 0.05, compared to the vehicle control. #p < 0.05, the comparison between two treatments as indicated. n.s.: no significant differences between two treatments.