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Fig. 5 | Journal of Nanobiotechnology

Fig. 5

From: Incorporation of drug efflux inhibitor and chemotherapeutic agent into an inorganic/organic platform for the effective treatment of multidrug resistant breast cancer

Fig. 5

The mechanisms of apoptosis in MCF7 and MCF7/MDR cells induced by NV@CaP-RGD. a We used JC-1 to mark the mitochondrial membrane potential and fluorescence microscopy and flow cytometry to measure that potential. The green fluorescence in the NV@CaP-RGD and NV@CaP groups increased significantly in MCF7 and MCF7/MDR tumor cells. b The mitochondrial membrane potential of the MCF7 cells and MCF7/MDR cells decreased significantly when treated with NV@CaP-RGD and NV@CaP, and there was no significant difference between these two groups. Control+ : carbonylcyanide-m-chlorophenylhydrazone, Control−: nontreated group (***P < 0.001, **P < 0.01, *P < 0.05 compared with the nontreated group). c The expression of apoptosis-related proteins ERK and p-ERK. Significant downregulation of the proteins ERK and p-ERK was detected by Western blotting analysis, suggesting that NV@CaP-RGD significantly induced apoptosis in MDR breast cancer cells via inhibition of the ERK signaling transduction pathway. According to the above results, NV@CaP-RGD promoted apoptosis in MDR breast cancer cells by decreasing the mitochondrial membrane potential and inhibiting ERK phosphorylation

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