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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: miR-22/KAT6B axis is a chemotherapeutic determiner via regulation of PI3k-Akt-NF-kB pathway in tongue squamous cell carcinoma

Fig. 3

Expression of the miR-22 target KAT6B and KAT6B knockdown sensitized tongue cancer cells to CDDP: a Schematic of the predicted miR-22 site in the human KAT6B 3′UTR, which is broadly conserved among vertebrates; b Inverse relationship between miR-22 and KAT6B mRNA and protein levels is shown; c and d miR-22 suppressed the activity of the luciferase gene linked to the 3′UTR of KAT6B, and a Renilla luciferase reporter was used for normalization. The data were obtained from three independent experiments. The mean of the results from CAl27 (c) transfected with the pMir-control and 293 T cells (d) transfected with the pMir-control and miR-22 were set as 100%, respectively. * p < 0.05. e The KAT6B expression change mediated by sh-KAT6B showed that sh-1# significantly reduced the KAT6B protein level; f Dose-inhibition rate curves were plotted from the MTS assay results collected from three independent experiments, showing that sh-1# significantly decreased cell viability upon CDDP treatment, with a left-shifted IC50 curve; g Western blot analysis revealed that sh-KAT6B enhanced CDDP-induced caspase 3 activation; h The effect of sh-KAT6B on CDDP-induced caspase3 activation in SCC9 cells. The relative activation of caspase3 was calculated from the average of three experiments. Each value is expressed as the ratio of the caspase3 activation level to the untreated level, and the untreated level was set as 1. *versus untreated, p < 0.05

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