Fig. 5: The AKT-NF-κB signalling pathway is the crucial mechanism of CD133 regulating MDR1/P-gp expression in CRC.
From: Targeting CD133 reverses drug-resistance via the AKT/NF-κB/MDR1 pathway in colorectal cancer
The AKT OE plasmid or the NF-κB/p65 OE plasmid could reverse the effects of CD133 KD plasmid in LoVo/ADR cells: a reversal of reduced P-gp expression in western blots; b reversal of reduced MDR1 mRNA expression by qPCR; c reversal of reduced MDR1 gene promoter activity by a luciferase reporter assay. d, e reversal of enhanced intracellular DOX concentrations; e reversal of reduced P-gp expression by immunofluorescence; f reversal of enhanced sensitivity in the CCK-8 assay; The AKT KD plasmid or the NF-κB/p65 KD plasmid could reverse the effects of CD133 OE plasmid in LoVo cells: a reversal of increased P-gp expression in western blots; b reversal of increased MDR1 mRNA expression by qPCR; c reversal of increased MDR1 gene promoter activity by a luciferase reporter assay. d, e reversal of reduced intracellular DOX concentrations; e reversal of increased P-gp expression by immunofluorescence; f reversal of reduced sensitivity in the CCK-8 assay; *p < 0.05, **p < 0.01. Each bar represents the mean ± SD of three independent experiments.
