Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1123866 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We have sequenced miRNA libraries from human embryonic, neural and foetal mesenchymal stem cells. We report that the majority of miRNA genes encode mature isomers that vary in size by one or more bases at the 3’ and/or 5’ end of the miRNA. Northern blotting for individual miRNAs showed that the proportions of isomiRs expressed by a single miRNA gene often differ between cell and tissue types. IsomiRs were readily co-immunoprecipitated with Argonaute proteins in vivo and were active in luciferase assays, indicating that they are functional. Bioinformatics analysis predicts substantial differences in targeting between miRNAs with minor 5’ differences and in support of this we report that a 5’ isomiR-9-1 gained the ability to inhibit the expression of DNMT3B and NCAM2 but lost the ability to inhibit CDH1 in vitro. This result was confirmed by the use of isomiR-specific sponges. Our analysis of the miRGator database indicates that a small percentage of human miRNA genes express isomiRs as the dominant transcript in certain cell types and analysis of miRBase shows that 5’ isomiRs have replaced canonical miRNAs many times during evolution. This strongly indicates that isomiRs are of functional importance and have contributed to the evolution of miRNA genes
2014-08-06 | GSE58734 | GEO
Project description:Small extracellular vesicles (sEVs) are critical mediators of tumour–microenvironment communication, largely through the selective transfer of microRNAs (miRNAs) that reprogram recipient cells. Active miRNA sorting into sEVs depends on RNA‑binding proteins, sequence determinants and RNA modifications. Here, a functional interplay between the RBP SYNCRIP and N6‑methyladenosine (m6A) RNA methylation in controlling miRNA loading into hepatocellular carcinoma (HCC)‑derived sEVs has been disclosed. It is reported that i) METTL3‑dependent m6A modification is required for efficient binding of SYNCRIP to specific miRNAs, thereby enabling their selective incorporation into sEVs; ii) silencing of SYNCRIP markedly reshapes the sEV miRNA-cargo and impairs the ability of HCC‑derived sEVs to induce epithelial–mesenchymal transition (EMT) in non‑tumorigenic hepatocytes. Notably, iii) depletion of METTL3 produces an even stronger effect, indicating that m6A methylation represents an upstream and essential determinant of SYNCRIP‑mediated miRNA export. Mechanistically, the data identify SYNCRIP as an m6A‑dependent miRNA reader, adding epitranscriptomic regulation to sequence‑based miRNA sorting into sEVs. Functionally, disruption of this interaction attenuates sEV‑driven EMT and pro‑tumorigenic signalling. Collectively, these findings uncover a novel regulatory axis governing sEV miRNA cargo selection and highlight the m6A–SYNCRIP interplay as a potential therapeutic target to interfere with EV‑mediated tumour progression and metastasis.
2026-06-12 | GSE317620 | GEO
Project description:Plasma miRNA profiling of nasopahryngeal carcinoma patients
| PRJNA210151 | ENA
Project description:MicroRNAs (miRNAs) in oral squamous cell carcinoma (OSCC)-derived small extracellular vesicles (sEVs) play a pivotal role in modulating intercellular communications between tumor cells and other cells in microenvironment, thereby influencing tumor progression and the efficacy of therapeutic interventions. However, a comprehensive inventory of these secretory miRNAs in sEVs and their biological and clinical implications remains elusive. This study aims to profile the miRNA content of OSCC cell lines sEVs and computationally elucidate their biological and clinical relevance. We conducted miRNA sequencing to compare the miRNA profiles of OSCC cells and their corresponding sEVs. Our motif enrichment analysis identified specific sorting motifs that are implicated in either cellular retention or preferential sEVs secretion. Target cell analysis suggested that the sEVs miRNAs potentially interact with various immune cell types, including natural killer cells and dendritic cells. Additionally, we explored the clinical relevance of these miRNAs by correlating their expression levels with TNM stages and patient survival outcomes. Intriguingly, our findings revealed that a distinct sEVs miRNA signature is associated with lymph node metastasis and poorer survival in patients in TCGA-HNSC dataset. Collectively, this research furthers our understanding of the miRNA sorting mechanisms in OSCC and underscores their clinical implications.
2024-02-07 | GSE254937 | GEO
Project description:This study aimed to characterize the miRNA expression profile of plasma-derived small extracellular vesicles (sEVs) from diabetic foot rats treated with tibial cortex transverse transport. Plasma sEVs were isolated from peripheral blood samples of diabetic foot rats treated with either tibial transverse transport or sham surgery, followed by small RNA sequencing. Differentially expressed miRNAs were analyzed to explore the potential regulatory mechanisms by which tibial transverse transport promotes diabetic wound repair, with particular focus on angiogenesis, inflammatory regulation, immune modulation, and tissue regeneration.
2026-07-04 | GSE337487 | GEO
Project description:To discover miRNAs implicate in PAPS pathogenesis, we isolated sEVs from plasma of PAPS patients, aPL patients (patients with positive antiphospholipid antibodies without thrombotic or obstretic complications) and control. Then, we extracted RNA total and we performed miRNA-sequencing.
2023-07-18 | GSE220791 | GEO
Project description:Ischemic cardiomyopathy (ICM), caused by acute myocardial infarction (AMI), is the most common type of chronic heart failure (HF). Treg cells, maintaining peripheral immune tolerance, are dysfunctional in ICM mice. The mechanism of dysfunctional Treg cells in ICM remains unclear. Furthermore, small extracellular vesicles (sEVs) are significant in intracellular communication and tissue homeostasis. This study tends to illustrate whether plasma sEVs of ICM promote the dysfunctional state of Treg cells through miRNA and thus aggravate cardiac remodeling.In ICM patients, the number of Treg cells was increased while Foxp3 mean fluorescence intensity (MFI) was decreased in peripheral blood, indicating a dysfunctional phenotype of Treg cells. miR-223-3p, identified by sequencing using plasma sEVs of ICM patients, was upregulated and negatively correlated with blood Treg cell number. Additionally, the number of cardiac Treg cells of ICM mice was increased while Foxp3 MFI was decreased. Furthermore, plasma sEVs from ICM mice aggravate ventricular remodeling in mice post-AMI. Besides, ICM-sEVs decreased the number of Treg cells while miR-223-3p knockdown increased the number of them and promoted the expression of Foxp3 in vitro.Plasma sEVs of ICM aggravate ventricular remodeling post-AMI through miR-223-3p-mediated Treg cells dysfunction in ICM.
2025-12-01 | GSE283390 | GEO