Gene expression changes induced by over-expression of miR-181b-5p in db/db mouse
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PROVIDER: PRJNA679782 | ENA |
REPOSITORIES: ENA
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Project description:Expression Signatures of diabetic mouse and miR-181b-5p overexpression in db/db mouse
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Project description:The microRNAs (miRNAs) that can influence diabetic kidney disease (DKD) have not been fully characterized. The aim of this study was to identify the miRNAs that affect DKD and could be used as specific biomarkers or therapeutic agents. First, kidneys from two DKD mouse models were screened for differences in miRNA expression from control mice. We found that miRNA-125b-5p and miRNA-181-5p were specifically differentially expressed in the kidneys of DKD mice. Next, we administered miRNA-181b-5p-mimic to DKD mice, which reduced the albuminuria and abnormal mesangial expansion. Pathway analysis revealed that overexpression of miRNA-181-5p significantly altered the expression of 51 genes in the kidneys of DKD mice. Furthermore, the serum level of miRNA-125b-5p was significantly higher and that of miRNA-181-5p was lower in patients with DKD than in patients with other kidney diseases. These results suggest that miRNA-125b-5p and miRNA-181b-5p may represent novel diagnostic biomarkers and that miRNA-181b-5p may represent a therapeutic target for DKD.
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Project description:This is a prospective-retrospective study to determine if the expression of the miRNA’s miR-31-3p and miR-31-5p are prognostic of patient outcomes or predictive of the benefit from anti-EGFR therapy in stage III Colon Cancer. The present study will utilize FFPE tumor samples collected from patients enrolled in the PETACC-8 study conducted by the Fédération Francophone de Cancérologie Digestive (FFCD). This phase 3 clinical trial prospectively randomized fully resected stage III colon cancer patients to receive adjuvant treatment with either FOLFOX-4 plus cetuximab or FLOFOX-4 alone.
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Project description:RNA-sequencing was performed to gain insight into the transcriptome-wide molecular changes induced by miR-30a-5p or miR-30a-3p over-expression in lung adenocarcinoma cells. Following transfection of miR-30a-5p or miR-30a-3p miRNA mimic or control RNA, RNA-sequencing was performed. This high-throughput data revealed elevated expression of both miR-30a-5p and miR-30a-3p reduced the expression of genes and pathways known to induce proliferation and movement in lung adenocarcinoma cells.
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Project description:MiRNAs have been shown to alter both protein expression and secretion in different cellular contexts. By combining in vitro, in vivo and in silico techniques, we demonstrated that overexpression of pre-miR-1307 reduced the ability of breast cancer cells to induce endothelial cell sprouting and angiogenesis. However, the molecular mechanism behind this and the effect of the individual mature miRNAs derived from pre-miR-1307 on protein secretion and is largely unknown. Here, we overexpressed miR-1307-3p|0, -3p|1 and 5p|0 in MDA-MB-231 breast cancer cells and assessed the impact of miRNA overexpression on protein secretion by Mass Spectrometry. Unsupervised hierarchical clustering revealed a distinct phenotype induced by overexpression of miR-1307-5p|0 compared to the controls and to the 5’isomiRs derived from the 3p-arm. Together, our results suggest different impacts of miR-1307-3p and miR-1307-5p on protein secretion which is in line with our in vitro observation that miR-1307-5p, but not the isomiRs derived from the 3p-arm reduce endothelial cell sprouting in vitro. Hence these data support the hypothesis that miR-1307-5p is at least partly responsible for impaired vasculature in tumors overexpressing pre-miR-1307.
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Project description:Meis1 is a transcription factor involved in a broad range of functions including development and proliferation and has been previously shown to harness cell cycle progression. This study aimed to investigate the regulation of Meis1 by long non-coding RNAs (lncRNAs) and their sponged microRNAs (miRNAs) and hence the impact of this regulatory axis on cell proliferation. Using in-silico analysis, miR-499-5p was predicted to target Meis1 and Malat1 was predicted and previously proven to sponge miR-499-5p. We showed that forcing the expression of miR-499-5p downregulates Meis1 expression in C166 cell line by directly binding to its 3’UTR. In addition, Malat1 knockdown significantly increases miR-499-5p expression, subsequently suppressing Meis1 mRNA and protein expression levels. Furthermore, the impact of manipulating the Malat1/miR-499-5p/Meis1 axis on cellular proliferation was assessed using the BrdU incorporation assay. We demonstrated that upon knockdown of Malat1, mimicking with miR-499-5p, or knockdown of Meis1, cell proliferation was induced. Gene Ontology, KEGG and Reactome enrichment analyses were performed on proteins detected by mass spectrometry following manipulation of the Malat1/miR-499-5p/Meis1 axis. The data revealed a multitude of differentially expressed proteins (DEPs) significantly enriched in processes related to cell cycle, cell division and proliferation. These DEPs were also involved in key signaling pathways, such as Wnt and mTOR, known to play critical roles in cell proliferation and cell cycle. Finally, since Malat1 and miR-499-5p are conserved in humans and mice, we examined the expression pattern of both non-coding RNAs (ncRNAs) in the hearts of neonatal, postnatal, and adult mice, representing models of proliferative and non-proliferative tissues. We demonstrated a paradoxical expression pattern, where Malat1 is underexpressed while miR-499-5p is overexpressed in proliferative neonatal cardiomyocytes. Collectively, our findings confirm that Malat1 sponges miR-499-5p which directly regulates Meis1, and that Malat1/miR-499-5p/Meis1 axis has a pivotal influence on cellular proliferation.
2025-05-07 | PXD054558 | Pride
Project description:Post-transcriptional regulation of gene expression by miRNAs likely makes significant contributions to mRNA abundance at the embryo-maternal interface. In this study, we investigated how miR-26a-5p and miR-125b-5p contribute to molecular changes occurring in the uterine luminal epithelium, which serves as the first site of signal exchange between the mother and developing embryo. To measure de novo protein synthesis after miRNA delivery to primary uterine luminal epithelial cells, we employed pulsed stable isotope labeling by amino acids (pSILAC). We found that both miRNAs alter the proteome of luminal epithelial cells, impacting numerous cellular functions, immune responses, as well as intracellular and second messenger signaling pathways. Additionally, we identified several features of miRNA-mRNA interactions that may influence the targeting efficiency of miR-26a-5p and miR-125b-5p. Overall, our study suggests a complex interaction of miR-26a-5p and miR-125b-5p with their respective targets. However, both appear to cooperatively function in modulating the cellular environment of the luminal epithelium, facilitating the morphological and molecular changes that occur during the intensive communication between the embryo and uterus at pregnancy.
2025-05-07 | PXD056243 | Pride
Project description:Analysis revealed a set of 13 microRNAs to be significantly altered between livers of control db/+ and diabetic db/db mice. Of these, miR-34a, miR-107, miR-378, miR-378*, miR-31, miR-31*, miR-151-5p, miR-676, miR-22, miR-93, let-7b were up-regulated and let-7e and miR-227 were down-regulated. A total of 670 predicted targets for these altered miRNAs were extracted from PicTar and TargetScan and functional characterisation mapped these targets to several biological processess related to varied metabolic pathways. The Wnt signaling pathway that has been shown to be linked to diabetes emerged as the most prominent pathway from these sets of target genes.
2011-12-22 | GSE17035 | GEO
Project description:The microRNAs (miRNAs) that can influence diabetic kidney disease (DKD) have not been fully characterized. The aim of this study was to identify the miRNAs that affect DKD and could be used as specific biomarkers or therapeutic agents. First, kidneys from two DKD mouse models were screened for differences in miRNA expression from control mice. We found that miRNA-125b-5p and miRNA-181-5p were specifically differentially expressed in the kidneys of DKD mice. Next, we administered miRNA-181b-5p-mimic to DKD mice, which reduced the albuminuria and abnormal mesangial expansion. Pathway analysis revealed that overexpression of miRNA-181-5p significantly altered the expression of 51 genes in the kidneys of DKD mice. Furthermore, the serum level of miRNA-125b-5p was significantly higher and that of miRNA-181-5p was lower in patients with DKD than in patients with other kidney diseases. These results suggest that miRNA-125b-5p and miRNA-181b-5p may represent novel diagnostic biomarkers and that miRNA-181b-5p may represent a therapeutic target for DKD.
2020-12-21 | GSE161884 | GEO
Project description:RNAseq of mouse arthritic ankles with over-expression of miR-17-5p
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