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. 2017 Dec 13;8:902. doi: 10.3389/fphar.2017.00902

FIGURE 4.

FIGURE 4

Overexpression of survivin contributes to the induction of hormone therapy resistance in the ER+ HDAC2-upregulated breast cancer cells. (A) MCF7 and ZR-75-1 cells were treated with 4 μM tamoxifen for 24–48 h and expression of survivin and conversion of LC3B-II were determined by Western blotting. (B) MCF7 and MCF7-TamC3 cells were transfected with either scramble siRNA or survivin siRNA for 72 h. Expression of survivin, Atg5-Atg12 conjugate, and conversion of LC3B-II were determined by Western blotting. Actin was used as an internal control. (C) Kaplan–Meier survival estimates of high (red line) or low (black line) survivin expression in ER+ endocrine therapy-treated breast cancer. (D) ROC analysis of BIRC5 (survivin) for 5-year relapse-free survival on ER+ tamoxifen-treatment breast cancer patients. (E) MCF7-TamC3 cells were pre-transfected with either scramble siRNA or survivin siRNA for 24 h and co-treated with or without tamoxifen for 72 h. Cell viability was assessed by the MTT assay. (F) MCF7-TamC3 cells were pre-transfected with either scramble siRNA or survivin siRNA for 24 h and subsequently cultured under either estrogen-containing (Full) or estrogen-deprived conditions for 72 h. (G) ZR-75-1 cells were pre-transfected with either scramble siRNA or survivin siRNA for 24 h and subsequently cultured under either estrogen-containing (Full) or estrogen-deprived conditions for 72 h. Cell viability was assessed by the MTT assay. “,∗∗, and “∗∗∗” denote a statistical significance (P < 0.05, P < 0.01, and P < 0.001, respectively) between the testing groups.