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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: ER-α36 mediates cisplatin resistance in breast cancer cells through EGFR/HER-2/ERK signaling pathway

Fig. 6

Disruption of ER-α36-mediated nongenomic estrogen signaling increases cisplatin sensitivity in breast cancer cells. a MCF-7 cells were treated with or without 5 μg/mL cisplatin (DDP) for 48 h after preincubated with or without AG1478, Lapatinib, and U0126 at the indicated concentrations for 6 h, respectively. Then the levels of ER-α36, total EGFR (EGFR) and phosphorylated EGFR (P-EGFR), total HER-2 (HER-2) and phosphorylated HER-2 (P-HER-2), total ERK (ERK) and phosphorylated ERK (P-ERK) were evaluated using western blot. b MCF-7 cells were treated as in (a), and then the cell proliferation was measured with CCK-8 assay kit. c MCF-7/ER-α36 cells were treated with 5 μg/mL cisplatin for 48 h after preincubated with or without AG1478, Lapatinib, and U0126 at the indicated concentrations for 6 h, respectively. Then the total ERK (ERK) and phosphorylated ERK (P-ERK) was detected by western blot. d MCF-7/ER-α36 cells were treated as in (c), and then the cell proliferation was examined using CCK-8 assay kit. *P < 0.05, **P < 0.01, ***P < 0.001

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