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. 2019 Sep 14;48:264–276. doi: 10.1016/j.ebiom.2019.09.016

Fig. 6.

Fig. 6

Genetic GPR4 inhibition suppressed CRC progression in vivo.

(a) Subcutaneous xenografts derived from shNC or shGPR4 HCT116 cells. (b) Tumour volume growth curves of the subcutaneous xenografts (n = 5). (c) Tumour weights of the subcutaneous xenografts (n = 5). (d) IHC staining for Ki67, Active RhoA -GTP, YAP1 and Myc in subcutaneous tumour sections. Scale bar, 100 μm. (e) Liver metastasis burden of mice injected with shNC or shGPR4 MC38 cells. (f) H&E staining of livers from shNC and shGPR4 MC38 mice. Scale bar, 500 μm. (g) Statistical analysis of liver weights and percentage of tumor invasive area (n=5). (h) IHC staining for Ki67, Active RhoA -GTP, YAP1 and Myc in liver metastasis tumour sections. (i) Survival of liver metastasis mice with shNC MC38 and shGPR4 MC38 tumours. (j) Organoid culture of colorectal cancer with the indicated treatment. (k) Model proposing that upregulated GPR4 promotes colorectal cancer progression in an acid tumour microenvironment. Differences between the groups in (b) were analysed by one-way ANOVA test (* P < .05; ** P < .01; *** P < .001). Differences between the groups in (c, g) were analysed by unpaired Student's t-test (* P < .05; ** P < .01; *** P < .001). Differences between two groups in (i) were analysed by log-rank test. (* P < .05; ** P < .01; *** P < .001).