Analysis of miRNA expression profiling in 3 samples(normal, cigarette smoking and lung cancer population's serum)
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ABSTRACT:
ORGANISM(S): synthetic construct Homo sapiens
PROVIDER: GSE58540 | GEO | 2014/06/17
SECONDARY ACCESSION(S): PRJNA252846
REPOSITORIES: GEO
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Project description:Using the highly sensitive miRNA array, we determined the serum miRNAs profiles of 10 non-smokers, 10 smokers and 10 lung cancer patients by miRCURY LNA™ microRNA Arrays. Differential expressed miRNAs were further validated in a larger scale samples. We found that let-7i-3p and miR-154-5p were significantly downregulation in serum of smokers and lung cancer patients. The serum level of let-7i-3p and miR-154-5p is associated with smoking and smoking-related lung cancer. In this study, we mix 10 samples with equal volume of each group(non-smoking control group,smoking group and lung cancer group ) and run RNA extractions. And then miRCURYTM LNA Array (v.16.0) was applied in the studying of miRNA expression profile and its alteration to gain the miRNA expression profile to compare the variety between each two groups respectively.
2014-06-17 | E-GEOD-58540 | biostudies-arrayexpress
Project description:ABSTRACT: OBJECTIVE. Smoking suppresses PD-1 expression in patients with rheumatoid arthritis (RA). In this study, we assess if smoking changed the epigenetic control over CD8+ T cell memory formation through a microRNA (miR) dependent mechanism. METHODS. Phenotypes of CD8+ T cells from smokers and non-smokers, RA and healthy, were analyzed by flow cytometry. A microarray analysis was used to screen for differences in miR expression. Sorted CD8+ cells were in vitro stimulated with nicotine and analyzed for transcription of miRs and genes related to memory programming by qPCR. RESULTS. CD27+CD107a–CD8+ T cells, defining a naïve-memory population, had low expression of PD-1. Additionally, the CD27+ population was more frequent in smokers (p=0.0089). Smokers were recognized by differential expression of 8 miRs. Let-7c-5p, let-7d-5p and let-7e-5p, miR-92a-3p, miR-150-5p and miR-181-5p were up regulated, while miR-3196 and miR-4723-5p were down regulated. These miRs were predicted to target proteins within the FOXO-signaling pathway involved in CD8+ memory programming. Furthermore, miR-92a-3p was differentially expressed in CD8+ cells with naïve-memory predominance. Nicotine exposure of CD8+ cells induced the expression of miR-150-5p and miR-181a-5p in the naïve-memory cells in vitro. Additionally, nicotine exposure inverted the ratio between mRNAs of proteins in the FOXO pathway and their targeting miRs. CONCLUSIONS. Smokers have a high prevalence of CD8+ T cells with a naïve-memory phenotype. These cells express a miR profile that interacts with the memory programming conducted through the FOXO pathway.
2020-06-29 | GSE146393 | GEO
Project description:The study integrated both miRNA and mRNA profiles to explore novel miRNA-mRNA interactions that affect the regulatory patterns in de novo CN-AML. A total of 637 significant negative correlations (FDR <0.05) were reported. Network analysis revealed a cluster of 12 miRNAs that represents the majority of the mRNA targets. Within the cluster, five miRNAs; miR-495-3p, miR-185-5p, let-7i-5p, miR-409-3p, and miR-127-3p were suggested to play a pivotal role in the regulation of CN-AML as they are associated with negative regulation of myeloid leukocyte differentiation, negative regulation of myeloid cell differentiation, positive regulation of haematopoiesis, and hematopoiesis and its regulation. Three novel interactions in CN-AML were predicted, let-7i-5p:HOXA9, miR-495-3p:PIK3R1 and miR-495-3p:CDK6 which are responsible in regulating myeloid cell differentiation in CN-AML.
2019-12-30 | GSE142699 | GEO
Project description:The study integrated both miRNA and mRNA profiles to explore novel miRNA-mRNA interactions that affect the regulatory patterns in de novo CN-AML. A total of 637 significant negative correlations (FDR <0.05) were reported. Network analysis revealed a cluster of 12 miRNAs that represents the majority of the mRNA targets. Within the cluster, five miRNAs; miR-495-3p, miR-185-5p, let-7i-5p, miR-409-3p, and miR-127-3p were suggested to play a pivotal role in the regulation of CN-AML as they are associated with negative regulation of myeloid leukocyte differentiation, negative regulation of myeloid cell differentiation, positive regulation of haematopoiesis, and hematopoiesis and its regulation. Three novel interactions in CN-AML were predicted, let-7i-5p:HOXA9, miR-495-3p:PIK3R1 and miR-495-3p:CDK6 which are responsible in regulating myeloid cell differentiation in CN-AML.
2019-12-30 | GSE142698 | GEO
Project description:Circulating microRNAs (miRNAs) in serum may serve as promising diagnostic biomarkers for patients with gastric cancer (GC). Using quantitative reverse transcription polymerase chain reaction (qRT-PCR) based Exiqon panel, we identified 58 differentially expressed miRNAs from 3 GC pool samples and 1 normal control (NC) pool in the initial screening phase. Identified miRNAs were further validated in the training (49 GC VS. 47 NCs) and validation phases (154 GC VS. 120 NCs) using qRT-PCR. Consequently, six serum miRNAs (miR-10b-5p, miR-132-3p, miR-185-5p, miR-195-5p, miR-20a-3p and miR-296-5p) were significantly overexpressed in GC compared with NCs. The areas under the receiver operating characteristic (ROC) curve of the six-miRNA panel were 0.764 and 0.702 for the training and validation phases, respectively. In conclusion, we identified a six-miRNA panel in serum for the detection of GC.
2016-08-31 | GSE86226 | GEO
Project description:From serum samples of non-dialyzed and dialyzed patients with ADPKD and healthy control total RNA was isolated and miRNA expression was evaluated. Circulating microRNAs (miRNA) are important intercellular communication compounds. We investigated the influence of ADPKD (autosomal dominant polycystic kidney disease) and hemodialysis on the profile of serum miRNAs. We found 37 significant circulating miRNA that differ between ADPKD patients (dialyzed and non-dialyzed) and healthy controls. Bioinformatic analysis revealed strongest connections between those miRNAs and KEGG pathway: MicroRNAs in cancer. We selected 3 miRNAs with highest and 3 with lowest fold change in comparison of dialyzed and non-dialyzed patients and compared their expression in paired pre-/post-dialysis samples. All up-regulated miRNAs (miR-532-3p, miR-320b, miR-144-5p) were not significantly altered by hemodialysis. From down-regulated miRNAs miR-27a-3p was shown to be significantly lower after dialysis in both total and exosomal fraction. MiR-20a-5p was down-regulated after dialysis only in the exosomal fraction whereas miR-16-5p was unaltered by hemodialysis. MiR-16-5p was selected as the best circulating biomarker of ADPKD with miR-22-3p, let-7i-5p and miR-24-3p as following best ones. Circulating representatives of miR-17 family (new drug target of ADPKD (Hajarnis et al. 2017)) sharing the same seed region (miR-20a-5p, miR-93-5p and miR-106a-5p) showed significantly lowered expressed in sera of dialyzed patients vs non-dialyzed ones and their exosomal fraction dropped after hemodialysis. We concluded that serum miRNA among ADPKD patients differ substantially depending on the stage of CKD. These alterations show possible links with cancer. The exosomal fraction of miRNA was more affected by dialysis than total fraction of miRNAs suggesting their dynamically changing functional role.
2018-06-30 | GSE101811 | GEO
Project description:COPD is a heterogeneous condition without effective disease modifying therapies. Identification of novel inflammatory endotype markers such as extracellular vesicles (EVs), which are important intercellular messengers carrying microRNA (miRNA), may enable earlier diagnosis and disease stratification for a targeted treatment approach. Our aim was to identify differentially expressed EV miRNA in the lungs of COPD patients compared with healthy ex-smokers and determine whether they can help define inflammatory COPD endotypes. EV miRNA were isolated and sequenced from ex-smoking COPD patients and healthy ex-smoker bronchoalveolar lavage fluid. Results were validated with RT-qPCR and compared to differential inflammatory cell counts. Differential expression analysis identified five upregulated miRNA in COPD (miR-223-3p, miR-2110, miR-182-5p, miR-200b-5p and miR-625-3p) and three downregulated miRNA (miR-138-5p, miR-338-3p and miR-204-5p), all with a log2 fold change of >1/-1, FDR<0.05. These miRNAs correlated with disease defining characteristics such as FEF 25-75% (a small airways disease measure) and DLCO % (a surrogate measure of emphysema). Receiver operator curve analysis demonstrated miR-2110, miR-223-3p and miR-182-5p showed excellent combinatory predictive ability (AUC 0.91, p<0.0001) in differentiating between health and mild COPD. Furthermore, miR-223-3p and miR-338-3p correlated with airway eosinophilia and were able to distinguish “pure eosinophilic” COPD from other airway inflammatory subtypes (AUC 0.94 and 0.85 respectively). This is the first study to identify differentially expressed miRNA in COPD bronchoalveolar lavage fluid EVs. These findings suggest specific lung derived EV miRNA are a strong predictor of disease presence even in mild COPD. Furthermore, specific miRNA correlated with inflammatory cell numbers in COPD, and may have a role in defining inflammatory endotypes for future treatment stratification.
2022-12-05 | GSE218571 | GEO
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.
2024-12-11 | PXD041087 | Pride
Project description:We report the differential expression of miRNA in serum exosome of heat strok patints. Compared with those from healthy volunteers, exosomes from patients with HS showed substantial changes in the expression of 202 exosomal miRNAs (154 upregulated and 48 downregulated miRNAs). The most upregulated miRNAs included miR-511-3p, miR-122-5p, miR-155-3p, miR-1290, and let7-5p, whereas the most downregulated ones included miR-150-3p, 146a-5p, and 151a-3p. Gene ontology enrichment of the miRNAs of patients with HS compared with control subjects were associated mostly with inflammatory response, including T cell activation, B cell receptor signaling, dendritic cell chemotaxis and leukocyte migration, and platelet activation and blood coagulation. The identified miRNAs were primarily enriched to the signal transduction pathways namely, T cell receptor signaling, Ras signaling, chemokine signaling, platelet activation, and leukocyte transendothelial migration, all of which are associated with inflammation and hemostasis. Multiple targeted mRNAs associated with the inflammatory response, blood coagulation, and platelet activation were further verified in serum exosomes. Exosomes from patients with HS convey miRNAs and mRNAs associated with pathogenic pathways, including inflammatory response and coagulation cascade. Exosomes may represent a novel mechanism for intercellular communication during HS.
2021-06-14 | GSE174224 | GEO
Project description:Background. Traditional combustion cigarette (TCC) smoking is an established risk factor for several types of cancer and cardiovascular diseases. Circulating microRNAs (miRNAs) represent key molecules mediating pathogenetic mechanisms, and potential biomarkers for personalized risk assessment. Several transcriptomics studies have showed that TCC smoking globally changes the profile of circulating miRNAs. The use of heat-not-burn cigarettes (HNBCs) as alternative smoking devices is rising exponentially worldwide, with still unknown long-term effects on health. Comprehensive data on the circulating miRNA profile in chronic HNBC smokers are still lacking. Purpose. We aimed at defining the profile of circulating miRNAs in serum samples of chronic exclusive HNBC smokers, and identifying potentially pathogenetic circulating miRNA signatures. Results. Differential expression analysis revealed 101 miRNAs significantly modulated between groups (adjusted p<0.05), with a prevalence of circulating miRNA downregulation in smokers (only 20 miRNAs were upregulated in both groups of smokers). Head-to-head comparison revealed that 65 miRNAs were exclusively modulated in TCC, 26 miRNAs were commonly modulated in both smoker groups, and 10 miRNAs were exclusively modulated in HNBC samples, all versus NS. KEGG pathway analysis performed on target genes of the commonly modulated miRNAs returned cancer-associated and cardiovascular disease pathways. The application of stringent abundance and fold-change criteria to this list nailed down our functional bioinformatic analyses to a network where miR-25-3p and miR-221-3p are main hubs for cardiovascular- and cancer- related molecular pathways, respectively. Conclusions. Our results define for the first time a global miRNA profile in the serum of exclusive chronic HNBC smokers. Despite the globally lower extent of the differences observed, our data suggest a significant detrimental impact of HNBCs on circulating miRNAs.
2023-06-13 | GSE233237 | GEO