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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: FOXQ1-mediated SIRT1 upregulation enhances stemness and radio-resistance of colorectal cancer cells and restores intestinal microbiota function by promoting β-catenin nuclear translocation

Fig. 4

Impact of FOXQ1 knockdown on the stemness and radio-resistance of CRC cells. A Western blot assay was used to screen out the most efficient sequence of FOXQ1 knockdown in HCT116R and HT29R cells; B Western blot assay was used to determine the changes in the protein expression of FOXQ1 after the treatment of sh-FOXQ1 and oe-FOXQ1 in HCT116R and HT29R cells; C The sphere formation assay was carried out to test the tumor sphere formation ability of HCT116R and HT29R cells in the presence of FOXQ1 knockdown/overexpression; D qRT-PCR was used to measure the mRNA expression of tumor stem cell markers (CD133, SOX2 and OCT4) in HCT116R and HT29R cells in the presence of FOXQ1 knockdown/overexpression; E MTT assay was carried out to test the cell viability of HCT116R and HT29R cells in response to FOXQ1 knockdown/overexpression (* p < 0.05 versus sh-NC-treated cells); F The colony formation assay to detect the colony formation ability of HCT116R and HT29R cells in response to FOXQ1 knockdown/overexpression; G Transwell assay to test the invasion ability of HCT116R and HT29R cells in response to FOXQ1 knockdown/overexpression; H Flow cytometry to detect the cell apoptosis of HCT116R and HT29R cells in response to FOXQ1 knockdown/overexpression. *means p < 0.05 in the comparison between two groups. All cell experiments were repeated for three times independently. The measurement data were expressed as mean ± standard deviation. Unpaired t test was adopted for the comparison between groups, repeated measures ANOVA was adopted for multi-group comparison, and Tukey’s test was selected for pairwise comparison within the group

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