Fig. 5

SH3BGRL enhances anti-cancer drug resistance in breast cancer cells. a Flow cytometry analysis of the indicated apoptotic MCF-7 and MDA-MB-453 cells with Annexin V/7-AAD staining upon Cisplatin treatment. b Flow cytometry analysis of the indicated apoptotic MCF-7 cells with or without SH3BGRL overexpression or apoptotic MDA-MB-453 cells with or without endogenous SH3BGRL knockdown after Herceptin and Cisplatin treatments at the indicated dose and time. c IC₅₀ analysis of Lapatinib in MCF-7 cells with or without SH3BGRL overexpression, or MDA-MB-453 cells with or without endogenous SH3BGRL knockdown. d Apoptotic analyses of the indicated MDA-MB-453 cells with or without endogenous SH3BGRL knockdown by Herceptin (200 μg, 96 h), AKT inhibitor LY294002 (Inhibitor, 40 μM, 24 h), the combination of Herceptin (200 μg) and AKT inhibitor LY294002 (40 μM, 24 h) for 48 h, the combination of Cisplatin (10 μM) and AKT inhibitor LY294002 (40 μM, 24 h) for 12 h, and the combination of Cisplatin (10 μM) and Herceptin (200 μg, 96 h) for 12 h. e Tumor growth curve induced by MDA-MB-453 cells (Vector) and SH3BGRL knockdown cells (SH3BGRL KD). Cells were injected subcutaneously, after one week injection, mice were cured with Lapatinib, Herceptin, LY294002, combination of LY294002 and Cisplatin, combination of Herceptin and LY294002 or DMSO via intraperitoneal injection twice a week. f Tumor weights with MDA-MB-453 cells (Vector) and SH3BGRL knockdown cells (SH3BGRL KD). Cells were injected subcutaneously and analyzed as above. All experiments were independently conducted for three times and data are shown as mean ± SEM. ^*p < 0.05; **p < 0.01; ***p < 0.001; ns means no statistical significance