Fig. 1

CXCR7 overexpression promotes EMT and upregulates the expression of DCLK1. A RNA-sequencing was performed in HCT116 cells infected with lentiviral expressed CXCR7 (LV-CXCR7) and control. Hierarchical clustering analysis of differentially expressing mRNAs between HCT116^Control and HCT116^LV−CXCR7. B Western blot analysis of the expression levels of CXCR7, DCLK1, E-cadherin, Vimentin, N-cadherin, ZEB1 and SANI1 in HCT116, SW620 and HT29 cells infected with LV-CXCR7 and control lentivirus or transfected with siCXCR7 and siNC. Statistical analysis was performed compared with control group normalized to β-actin. Bars are means ± SD, *P < 0.05, **P < 0.01, ***P < 0.001, n = 3. C, D RT-qPCR was performed to determine the mRNA levels of CXCR7, E-cadherin, Vimentin and DCLK1 in HCT116, HT29 and SW620 cells overexpressing or knockdown of CXCR7. Statistical analysis was performed compared with control group. Bars are means ± SD, *P < 0.05, **P < 0.01, ***P < 0.001, n = 3. E The correlation of CXCR7 (ACKR3) with Vimentin and DCLK1 was determined in CRC tissues by Gene Expression Profiling Interactive Analysis (GEPIA) online tools. F The overall survival analysis of gastrointestinal cancer patients (gastric adenocarcinoma plus colorectal adenocarcinoma) divided by expression of Vimentin and DCLK1 using GEPIA. The patients were divided with high and low gene expression levels using the median cutoff and log-rank P value was shown