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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

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. 6

Impact of FOXQ1 knockdown or SIRT1 overexpression on the stemness and radio-resistance of CRC Cells. A qRT-PCR was used to determine the mRNA expression levels of FOXQ1 and SIRT1 in HCT116R and HT29R cells in response to SIRT1 overexpression or FOXQ1 knockdown or their combination; B Tumor sphere formation assay was carried out to detect the tumor sphere formation ability of HCT116R and HT29R cells in response to SIRT1 overexpression or FOXQ1 knockdown or their combination; C qRT-PCR was used to determine the mRNA expression levels of CD133, SOX2 and OCT4 in HCT116R and HT29R cells in response to SIRT1 overexpression or FOXQ1 knockdown or their combination; D MTT was carried out to test the viability of HCT116R and HT29R cells in response to SIRT1 overexpression or FOXQ1 knockdown or their combination; E Colony formation assay was carried out to test the clone formation ability of HCT116R and HT29R cells in response to SIRT1 overexpression or FOXQ1 knockdown or their combination; F Transwell was carried out to test the invasive ability of HCT116R and HT29R cells in response to SIRT1 overexpression or FOXQ1 knockdown or their combination; G Flow cytometry was carried out to test the apoptosis of HCT116R and HT29R cells in response to SIRT1 overexpression or FOXQ1 knockdown or their combination. * p < 0.05 compared with sh-NC + oe-NC group, # p < 0.05 compared with sh-FOXQ1 + oe-NC group. All cell experiments were repeated for three times independently. The measurement data were expressed in mean ± standard deviation. One-way or repeated measurement ANOVA was used for multi-group comparison, and Tukey’s test was selected for pairwise comparison within the group

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