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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: Acetyltransferase NAT10 regulates the Wnt/β-catenin signaling pathway to promote colorectal cancer progression via ac4C acetylation of KIF23 mRNA

Fig. 6

The NAT10/KIF23 axis regulates CRC cells and GSK-3β/NAT10/KIF23/GSK-3β loop participants in the progression. A Correlation analysis between the protein level of β-catenin and NAT10 or KIF23 detected by IHC. B The expression of GSK-3β, phosphorylated GSK-3β and β-catenin were determined by WB upon NAT10 knockdown or overexpression in CRC cells. C The level of β-catenin in the cell nucleus and cytoplasm was determined by WB in SW480 and HT-29 cells. D β-catenin nuclear translocation and KIF23 were detected by IF staining upon NAT10 knockdown in SW480 cells. E IHC staining of xenograft tumors. The expression of β-catenin and KIF23 were detected by IHC. F The expression of GSK-3β, phosphorylated GSK-3β, and β-catenin along with NAT10, KIF23, and the downstream genes of β-catenin (Cyclin D1, c-Myc, Survivin, and Bcl-xL) were detected by WB in relatively treated cells. G NAT10 and KIF23 were detected by IF staining with or without the treatment of LiCl (20 mmol/L) in SW480 cells for 48 h. H RIP and acRIP followed by qPCR with or without the treatment of LiCl (20 mmol/L) in SW480 cells for 48 h. I The expression of NAT10, KIF23, GSK-3β, phosphorylated GSK-3β, and β-catenin was detected by WB with or without the treatment of LiCl (20 mmol/L) in SW480 and HT-29 cells for 48 h. Data are shown as mean ± SD of three independent experiments, *P < 0.05

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