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Fig. 5 | Cancer Cell International

Fig. 5

From: METTL3 promotes glycolysis and cholangiocarcinoma progression by mediating the m6A modification of AKR1B10

Fig. 5

Whole-transcriptome sequencing reveals that AKR1B10 is a target of METTL3. A Volcano plots showing DEGs between METTL3-overexpressed and Vector groups by transcriptome sequencing in RBE cells (n = 3). Red dots means gene upregulated in METTL3-overexpressed group compared with the Vector group, such as AKR1B10; green dots means downregulated in METTL3-overexpressed group compared with the Vector group. B Bubble plot of KEGG enrichment of the upregulated DEGs between the METTL3-overexpressed and Vector groups in RBE cells. C RT‒qPCR verification of transcriptome sequencing results. Four upregulated DEGs between the METTL3-overexpressed and Vector groups were selected. D The results of MeRIP-qPCR in the OE-METTL3 and Vector groups for four candidate DEGs. E The protein expression of AKR1B10 in RBE cells upon METTL3 overexpression was detected by western blotting. F Five potential m6A modification sites on AKR1B10 mRNA predicted by the SRAMP database. G The binding relationship between METTL3 and AKR1B10 was detected by RIP assays. H The effect of METTL3 overexpression on the stability of AKR1B10 mRNA was measured by actinomycin D. I The m6A modification site of METTL3 on AKR1B10 mRNA was explored by using a luciferase reporter assay. ns means P > 0.05, *Means P < 0.05, **means P < 0.01, ***means P < 0.001

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