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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: A patient-derived organoid-based study identified an ASO targeting SNORD14E for endometrial cancer through reducing aberrant FOXM1 Expression and β-catenin nuclear accumulation

Fig. 3

SNORD14E recruits SRSF1 and affects FOXM1 alternative splicing. A Heatmap of differentially expressed mRNAs in RNA-seq of HEC-1B cells with or without SNORD14E overexpression. B Volcano plot of differentially expressed genes between SNORD14E and control. Red dots represent upregulated genes, blue dots represent downregulated genes, and gray dots represent genes that were not differentially expressed. C AS events following SNORD14E overexpression. SE event accounts for the most (75%). D Venn diagram showing significantly differential expressing genes in TCGA-UCEC cohort and differential AS events caused by SNORD14E in RNA-seq. E RT-qPCR of RNA immunoprecipitation (RIP) assay for detecting the enrichment of SNORD14E on AS factors SRSF1, U2AF1, and SF3B1. IgG was used as negative control. F RT-qPCR of the anti-SRSF1 RIP assay showed the interaction between SRSF1-SNORD14E complex and FOXM1 mRNA. * P < 0.05, ** P < 0.01, *** P < 0.001. Skipped exon (SE), retained intron (RI), alternative 5’ splice site (A5SS), alternative 3′ splice site (A3SS), mutually exclusive exon (MXE)

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