Fig. 3: Identification of HNRNPC targets by high-throughput RNA-seq and MeRIP-seq. | Cell Death & Disease

Fig. 3: Identification of HNRNPC targets by high-throughput RNA-seq and MeRIP-seq.

From: The m6A reader HNRNPC promotes glioma progression by enhancing the stability of IRAK1 mRNA through the MAPK pathway

Fig. 3

A The graphs of m6A peak distribution showing the proportion of m6A peaks in the indicated regions in negative control and si-HNRNPC U251 cells. B Volcano plot of RNA-seq results after HNRNPC knockdown in U251 cells. Red dots indicate up-regulated genes and blue dots represent down-regulated genes, |log2 (FC)| ≥ 1, p < 0.05. C The quadrant diagram graph shows the significant difference of m6A peaks in the MeRIP-seq analysis and mRNA expression in the RNA-seq analysis after HNRNPC knockdown in U251 cells. D KEGG pathway enrichment analysis of differentially expressed genes after HNRNPC knockdown in U251 cells. E Western blot analysis of MAPK pathway relative protein levels in HNRNPC-knockdown U251 cells and HNRNPC-overexpressing U87 cells. F Venn diagram showing 19 genes in the MAPK pathway exhibiting significant differences in m6A peaks and mRNA expression. G Spearman correlation analysis predicting the correlation between the expression of HNRNPC and three candidate genes (IRAK1, PDGFA and MAP3K14) in TCGA database. H RT-qPCR analysis validated three candidate genes in U251 cells after HNRNPC knockdown. Data are shown as the mean ± SD of three replicates; **p < 0.01, ***p < 0.001, compared with the negative control group.

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