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Fig. 2 | Molecular Cancer

Fig. 2

From: METTL3 facilitates tumor progression via an m6A-IGF2BP2-dependent mechanism in colorectal carcinoma

Fig. 2

Identification of METTL3 targets via MeRIP-seq and RNA-seq. a, Immunoblotting of METTL3 in SW480 and SW620 cells (left), and in METTL3 knockdown SW620 and control SW620 cells (right). b, Distribution of peaks (fold change > 1.5 or < − 1.5, P < 0.05) with a significant change in both the RNA expression level and m6A level in SW620 cells compared with SW480 cells (left), and in METTL3 knockdown SW620 cells compared to control SW620 cells (right). c, Venn diagram showing the shared peaks between metastatic-related hyper-up peaks and METTL3-related hypo-down peaks. A total of 192 shared peaks corresponding to 158 specific genes were observed. d, GO biological process enrichment analysis of the above shared peaks. e, The m6A abundances in SEMA3A, BCHE, ZFP36L2, and SOX2 transcripts in SW620 cells related to the SW480 cells (left panel), and in METTL3-knockdown SW620 cells (shMETTL3#1) related to the control SW620 cells (shNC) (right panel). f, Gene-specific m6A qPCR analysis of alterations in the m6A level in four representative genes in SW620 and SW480 cells. g, Gene-specific m6A qPCR analysis of alterations in the m6A level in four representative genes in METTL3-knockdown SW620 and control SW620 cells. h, Immunoblotting assay of SOX2 after METTL3-knockdown in SW620 and HCT116 cells. The data in f, and g are presented as the mean ± SDs (n = 3). *P < 0.05, **P < 0.01 (Student’s t-test). β-Actin was used as the loading control. The relative m6A level was normalized by input. The relative expression level was normalized by the β-Actin

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