Fig.7

HMOX1 and PRSS8 are post-transcriptionally regulated by miR-24-3p. A Volcano plot showing differentially expressed genes in HCT116 treated with a 100 nM miR-24 inhibitor relative to scramble control. Genes filtered for expression > 500 normalized counts in either condition. Horizontal dashed line represents p-adj cutoff of 0.05 (DESeq2). B Scatterplot of predicted miR-24-3p target genes that are upregulated (DESeq2 p-adj < 0.05, > 500 normalized counts in either condition) following miR-24-3p inhibition (n = 70). Vertical red line represents 1.5 × fold change. Genes in red exhibit > 1.5 × fold change (n = 6). Genes significantly downregulated in TCGA tumor tissue compared to non-tumor are represented by triangles (n = 9). Remaining genes represented by circles. (C) KEGG pathway enrichment analysis of 70 genes in (B). Pathways with p-value < 0.05 represented in figure. Color represents the -log10 p-value. D Normalized expression from RNA-seq counts for HMOX1 and PRSS8 in TCGA colon tumor relative to non-tumor tissue. Significance determined by two-sided Wilcoxon test. E RT-qPCR for HMOX1 and PRSS8 following 100 nM miR-24 inhibitor or scramble treatment in HCT116 cells. Significance determined by two-tailed Welch t-test. Color of data points represents experimental replicate. F RT-qPCR for HMOX1 and PRSS8 following HCT116 treatment with 50, 100 or 150 nM miR-24 mimic or scramble. Significance determined by two-tailed Student’s t-test. A non-parametric test was applied (two-sided Wilcoxon test), but significance couldn't be achieved due to low sample size. G DESeq2 normalized RNA-seq and ChRO-seq counts for HMOX1 and PRSS8 expression following HCT116 treatment with scramble or miR-24 inhibitor. Significance determined by two-tailed Welch t-test. *p < 0.05, **p < 0.01, ***p < 0.001