Fig. 7: m6A modification induced by FTO upregulates KDM5B. | Cell Death Discovery

Fig. 7: m6A modification induced by FTO upregulates KDM5B.

From: KDM5B promotes SMAD4 loss-driven drug resistance through activating DLG1/YAP to induce lipid accumulation in pancreatic ductal adenocarcinoma

Fig. 7: m6A modification induced by FTO upregulates KDM5B.

A Immunoblotting was used to detect the expression of indicated m6A demethylases and methylases in cells isolated from PDX mice of 2 and 3 passages treated with or without GEM. B Representative IHC staining images for FTO in tumor tissue from PDX treated with or without GEM. C A immunofluorescence assay was performed to detect the localization of FTO and KDM5B in BxPC-3 cells. D Scatter plot analysis of correlation between mRNA levels of FTO and KDM5B in 65 PDAC tissues. E Comparison of FTO expression in PDAC tissues of 12 patients with paired pericarcinomatous normal tissues. F MeRIP-qPCR results showed that the m6A enrichment of KDM5B was higher in BxPC-3 and Capan-1 cells than in HPDE6C7 cells. Effect of FTO overexpression in Capan-1 cells (G) and knockdown in BxPC-3 cells (H) on the expression of KDM5B. I Effect of FTO silencing the degree of m6A enrichment of KDM5B. J Effect of FTO silencing and overexpression on KDM5B stability in the presence of actinomycin. K RIP assay confirms the binding between YTHDF2 and KDM5B using anti-YTHDF2 antibodies in BxPC-3 and Capan-1 cells. L Protein level of KDM5B in PDAC cells was affected by the m6A binding proteins YTHDF2. M Effect of YTHDF2 silencing and overexpression on KDM5B stability in the presence of actinomycin. N Knockdown of FTO increased the m6A methylation in KDM5B mRNA by the YTHDF2-RIP analysis.

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