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Keywords {🔍}

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Topics {✒️}

n6-methyladenosine upregulates mir-181d-5p 250 ng/ul murine r-spondin mir-23a/mir-24/mir-27a cluster targeting yap1/tead4-ctgf axis small rna-seq data produced crispr/cas9 chromosome rearrangement crispr-cas9–mediated engineering microrna-34a expression profile celltiter-glo/cell count analyses mir-24-3p lna inhibitor regulating cdx2/heph axis drive inter-tumor heterogeneity article download pdf rna-induced silencing complex chro-seq library preparation c-myc-mediated inhibition cutaneous t-cell lymphoma recombinant human tgf-b1 real-time pcr small rna-seq data drive mir-375-3p expression tgf-beta receptor inactivation rna-seq data produced chro-seq data produced kraslsl−g12d conditional model mir-24-3p inhibition leads comprehensive microrna analysis β-catenin regulates effects tailed welch t-test mir-24-3p predicted targets predicted mir-24-3p targets tcga small rna-seq adding 5 ng/ml tgfb1 mir-24-3p increases apoptosis investigating fecal mir-24-3p ctgf-egfr signaling pathway mir-24-3p inhibitor exhibit small rna-sequencing data cre/crispr gene editors mir-24-3p inhibitor relative mir-10b inhibits metastasis suppress jak2/stat3 pathway shapiro–wilk test p gov/geo/query/acc 1 ml 50 mm tris–hcl mir-24-3p inhibitor treatment map3k8/erk signaling pathways genetically modified enteroids 1 ng/ml tgf-b1 beta-catenin-independent pathway

Questions {❓}

• Heterogeneity in Colorectal Cancer: A Challenge for Personalized Medicine?

Schema {🗺️}

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      headline:Comprehensive microRNA analysis across genome-edited colorectal cancer organoid models reveals miR-24 as a candidate regulator of cell survival
      description:Somatic mutations drive colorectal cancer (CRC) by disrupting gene regulatory mechanisms. Distinct combinations of mutations can result in unique changes to regulatory mechanisms leading to variability in the efficacy of therapeutics. MicroRNAs are important regulators of gene expression, and their activity can be altered by oncogenic mutations. However, it is unknown how distinct combinations of CRC-risk mutations differentially affect microRNAs. Here, using genetically-modified mouse intestinal organoid (enteroid) models, we identify 12 different modules of microRNA expression patterns across different combinations of mutations common in CRC. We also show that miR-24-3p is aberrantly upregulated in genetically-modified mouse enteroids irrespective of mutational context. Furthermore, we identify an enrichment of miR-24-3p predicted targets in downregulated gene lists from various mutational contexts compared to WT. In follow-up experiments, we demonstrate that miR-24-3p promotes CRC cell survival in multiple cell contexts. Our novel characterization of genotype-specific patterns of miRNA expression offer insight into the mechanisms that drive inter-tumor heterogeneity and highlight candidate microRNA therapeutic targets for the advancement of precision medicine for CRC.
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