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

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. Overall design: LEPC-Control, biotin-LEPC-miR-93-5p and LEPC-miR-93-5p-Mutation group mRNA profiles and miRNA interacting mRNA profiles were generated by deep sequencing, using Illumina Hiseq2500; H3K4me3, H3K27me3 and H3K9me3 ChIP-seqs were did in scr and miR-93-5p overexpressed LEPC cell lines.