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MiR-93-5p is a bona fide Oncodriver Targeting both Classical and Epigenetic Tumor Suppressive Pathways in Liver Cancer

ABSTRACT: Purpose: The goals of this study are to compare the transcriptome profiling among LEPC-Control, LEPC-Biotin-miR-93-5p and LEPC-Biotin-miR-93-5p-Muttion group to elevate the enrichment mRNA by Biotin-miR-93-5p in LEPC cells. Methods: LEPC-Control, LEPC-miR-93-5p and LEPC-miR-93-5p-MDX cells mRNA profiles were generated by deep sequencing, in triplicate, using Illumina Hiseq2500/Miseq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: we set the increase by ≥ 4 fold and transcripts at an FPKM ≥1 in LEPC cells as significance. By stepwise analysis, we identifies 615 high confident miR-93-5p-targted mature mRNA that is selectively enriched by biotin-miR-93-5p, but not biotin-miR-93-5p mutant, the miR-93-5p targetome we identified by HITS-CLSBP has 97.4% overlap with online predicted miR-93-5p mRNA targets. Conclusions: Overexpression of miR-93-5p instigates the malignant transformation of LEPC by regulating multiple cancer-related pathways.

ORGANISM(S): Mus musculus

PROVIDER: GSE93553 | GEO | 2019/01/12

REPOSITORIES: GEO

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Project description:Sepsis remains a leading cause of death and currently has no pathogenesis-specific therapy. Hampered progress is partly due to the lack of insight into deep mechanistic processes. Deciphering the functions of microRNAs in sepsis pathogeny became a dynamic research topic in the last decade. To screen for new microRNA targets for sepsis therapeutics, we used human samples: microRNA array data from peripheral blood mononuclear cells (PBMCs) from sepsis patients and controls, whole blood samples from sepsis survivors; and multiple animal models: mouse cecum ligation-puncture (CLP)-induced sepsis, mouse viral microRNA challenge, and baboon Gram-positive and Gram-negative sepsis models. miR-93-5p met the criteria for a therapeutic target, being overexpressed in baboons which died early after induction of sepsis and downregulated in humans who survived after sepsis. Therapeutically, inhibiting miR-93-5p prolonged the overall survival of mice with CLP-induced sepsis, with a stronger effect in old mice. Mechanistically, anti-miR-93-5p therapy reduced inflammatory monocytes and increased circulating effector memory T cells, especially CD4+ subset. Ago2-immunoprecipitation in miR-93-knockout T cells identified important regulatory receptors, CD28 and CD160, as direct miR-93-5p target genes. In conclusion, miR-93-5p is a potential therapeutic target in sepsis in the elderly through its regulation of both innate and adaptive immunity. We applied the Ago2-RIP Chip (Ribonucleoprotein ImmunoPrecipitation followed by microarray analysis) to identify miR-93-5p target mRNAs. This methodology uses beads coupled to either anti-Ago2 antibody (or an IgG control) to pull down the RISC complex together with any miRNA-interacting mRNAs. To define target genes of miR-93-5p, we assessed mRNA transcripts enriched in the Ago2-IP fraction of JURKAT parental cells or control cells (where miR-93-5p is present) but not in the two KO clones (where miR-93-5p is absent) by microarray

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MiR-93-5p is a bona fide Oncodriver Targeting both Classical and Epigenetic Tumor Suppressive Pathways in Liver Cancer

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