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Next Generation Sequencing of transcriptomes in GFP+-HSCs sorted from bone marrow of mice receiving HSCs subjected to control RNA or miR-31-5p inhibitor treatment.

ABSTRACT: Purpose: The goals of this study is to uncover the difference of transcriptomes that are essential for HSCs malignant transformation driven by miR-31-5p inhibition. Methods: GFP+-HSCs sorted from bone marrow mRNA profiles of mice receiving HSCs subjected to control RNA or miR-31-5p inhibitor treatment were generated by deep sequencing, using Illumina NovaSeq 6000 sequencer for 318 cycles.Reads that passed the Illumina quality filters were kept for the subsequent analyses. Adapters were trimmed from the reads, and reads shorter than 17 nt were discarded. The reads were mapped to the Mouse mRNA reference database using FANSe3 algorithm on Chi-Cloud NGS Analysis Platform (Chi-Biotech Co. Ltd., Shenzhen, China). Results: We use edgeR to analysis with a |log2 (FoldChange)| > 1 and p value <0.01. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to promote HSCs malignant driven by miR-31-5p inhibition. Conclusions: Our study represents the first detailed analysis of transcriptomes that promote T-cell malignant transformation driven by HTVL-1 oncogene Tax.

ORGANISM(S): Mus musculus

PROVIDER: GSE163985 | GEO | 2023/12/29

REPOSITORIES: GEO

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Next Generation Sequencing of WT, ORP4L KI, Wild-type, LCK/R26Tax, ORP4Lcko;LCK/R26Tax T-cells Transcriptomes.

Project description:Purpose: The goals of this study is to uncover the cellular pathways that are essential for T-cell malignant transformation driven by ORP4L and HTLV-1 oncogene Tax. Methods: T-cell mRNA profiles of WT, ORP4L KI, Wild-type, LCK/R26Tax, ORP4Lcko;LCK/R26Tax mice were generated by deep sequencing, using Illumina NovaSeq 6000 sequencer for 318 cycles.Reads that passed the Illumina quality filters were kept for the subsequent analyses. Adapters were trimmed from the reads, and reads shorter than 17 nt were discarded. The reads were mapped to the Mouse mRNA reference database using FANSe3 algorithm on Chi-Cloud NGS Analysis Platform (Chi-Biotech Co. Ltd., Shenzhen, China). Results: We use edgeR to analysis ORP4kI-vs-WT, LCK/R26Tax-vs-Wild-type，ORP4Lcko;LCK/R26Tax-vs-Wild-type，with a |log2 (FoldChange)| > 1 and p value <0.01. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to promote T-cell malignant. Conclusions: Our study represents the first detailed analysis of transcriptomes that promote T-cell malignant transformation driven by HTVL-1 oncogene Tax.

2023-11-11 | GSE162074 | GEO

Expression data from HSCs

Project description:Hepatic stellate cells (HSCs) experience phenotypic transformation, from the quiescent phenotype to the activated one, after different etiologies of liver injury. Liver fibrosis is then occurred upon the activation of HSCs. miR-16 deficiency is identified to be an important characteristic of HSCs activation. We used Affymetrix rat 230 2.0 arrays (Affymetrix, Santa Clara, U.S.A.) to uncover the global alternations of transcriptome under miR-16 restoration. We isolated quiescent hepatic stellate cells (HSCs) from adult male SD rats (normal control group) by in situ perfusion and density-gradient centrifugation. Activated HSCs were separated from rats of fibrosis model group, which were treated by 40% carbon tetrachloride (CCl4) for 8 weeks, by means of liver section, digestion and sequential centrifugation. Quiescent and activated HSCs were then divided into 4 groups at random, namely quiescent HSCs, activated HSCs, pLV-miR-16-treated HSCs and pLV-GFP-treated HSCs. The pLV-miR-16-treated group, pLV-GFP-treated group were infected with pLV-miR-16 and pLV-GFP, respectively.

2012-08-28 | E-GEOD-40381 | biostudies-arrayexpress

Expression data from HSCs

2012-08-28 | GSE40381 | GEO

Gene expression profiles of U87 cells after transfection with hsa-miR-145-5p and 31-5p

Project description:We analyzed the expression profiles of hsa-miR-145-5p or hsa-miR-31-5p-targeting genes relating to invasion or migration after co-overexpression of hsa-miR-145-5p and 31-5p Gene expression profiles of U87 cells after co-transfection with hsa-miR-145-5p and 31-5p mimics, and U87 cells after transfection miR mimic negative control

2016-06-23 | E-GEOD-83643 | biostudies-arrayexpress

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

Project description: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.

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Gene expression profiling of LT-HSCs and ST-HSCs conditionally expressing MLL-ENL

Project description:We have developed a new conditional transgenic mouse showing that MLL-ENL, at an endogenous-like expression level, induces leukemic transformation selectively in LT-HSCs. To investigate the molecular mechanism of leukemic transformation in LT-HSCs conditionally expressing MLL-ENL, we preliminarily performed comprehensive gene expression profiling of CreER-transduced LT-HSCs and ST-HSCs using cDNA microarray analysis. For initial screening of candidate genes invloved in the leukemic transformation, total RNA was extracted from colony-forming cells derived from LT-HSCs and ST-HSCs transduced with CreER or mock. Four samples were analyzed, and CreER-transduced LT/ST-HSC-derived cells were compared with mock-transduced LT/ST-HSC-derived cells, while CreER/mock-transduced LT-HSC-derived cells were compared with CreER/mock-transduced ST-HSC-derived cells.

2013-07-17 | E-GEOD-48539 | biostudies-arrayexpress

Gene expression profiling of LT-HSCs and ST-HSCs conditionally expressing MLL-ENL

2013-07-17 | GSE48539 | GEO

PETACC-8 miR-31-3p and miR-31-5p Ancillary Study

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