Skip to main content


Springer Nature is making Coronavirus research free. View research | View latest news | Sign up for updates

Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Co-delivery of sorafenib and metapristone encapsulated by CXCR4-targeted PLGA-PEG nanoparticles overcomes hepatocellular carcinoma resistance to sorafenib

Fig. 1

Effect of sorafenib, metapristone and their combination treatment on HCC cells proliferation. After treatment for 24 h and 48 h, the cell viability of SMMC-7721, HepG2 and Huh7 cells was inhibited by sorafenib (a) and metapristone (b) in a dose-dependent manner. Data are expressed as the mean ± SD (n = 5). After 24-h treatment, metapristone induced a remarkable decline of CXCR4 at the mRNA level (c) and at the protein level (d). The data were shown by western blot images (left panels) and quantitative analysis (right panels). Data are expressed as the mean ± SD (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001. e The combination treatment of sorafenib (0, 2, 5, 8, 10 and 15 μM) with metapristone (0, 10, 25 and 50 μM) enhanced anti-proliferative effect in SMMC-7721 cells, as compared with either drug alone. Data are expressed as the mean ± SD (n = 5). Compared with the metapristone monotherapy group, *P < 0.05, **P < 0.01, ***P < 0.001; Compared with the sorafenib monotherapy group, #P < 0.05, ##P < 0.01, ###P < 0.001. f The combined effect of sorafenib (2, 5, 8, 10 and 15 μM) and metapristone (50 μM) was determined by CI values, which was calculated from the fraction-affected value of each combination using Compusyn software. CI > 1, antagonism; CI = 1, additive effect; CI < 1, synergism. All experiments were repeated at least three times

Back to article page