Fig. 4

NV@CaP-RGD substantially promoted apoptosis and improved the therapeutic effect on MCF7/MDR cells. a An annexin V/PI double-staining assay was used to evaluate the apoptotic ratio of MCF7/MDR cells treated with unbound VRP-NVT, NV@CaP-RGD and NV@CaP for 72 h. b Quantitative analysis of the apoptosis ratio. Compared to unbound VRP-NVT, NV@CaP-RGD and NV@CaP were better able to induce apoptosis of MCF7/MDR cells, including early and late apoptosis, but no significant difference was found between these two groups (***P < 0.001 compared with the control group). The codelivery of VRP and NVT by NPs had a synergistic effect on the induction of apoptosis in MCF7/MDR cells. EA indicates early apoptosis, LA indicates late apoptosis, and TA indicates total apoptosis. c Cell viability of MCF7/MDR cells treated with various concentrations of unbound VRP-NVT, NV@CaP and NV@CaP-RGD for 72 h (***P < 0.001, **P < 0.01, *P < 0.05, compared with the control group). The cell viability significantly decreased in the NV@CaP-RGD and NV@CaP groups, suggesting that NV@CaP-RGD was able to effectively inhibit the viability of MDR breast cancer cells at the cellular level