Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA122009 | ENA |
REPOSITORIES: ENA
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Project description:HaCaT human keratinocytes were transfected with pre-miR-483-3p or pre-miR-NC. RNA samples were harvested 48h post-transfection and mRNA profiles were determined with pan genomic arrays. Two biological replicates were performed for each comparison. Data were normalized using a dye-swap method.
2011-06-29 | GSE19931 | GEO
Project description:MicroRNA-483 (miR-483) regulate endothelial function through inhibition expression of connective tissue growth factor (CTGF). Endothelial dysfunction is involved in the pathogeneis of pulmonary arterial hypertension (PAH). We investigated the role of miR-483 overexpression on human pulmonary arterial endothelial cells (hPAECs) through comparing the transcriptome file of hPAECs transfected with miR-483 -3p and -5p mimic and with control mimic. Gene ontology analysis showed that several PAH-associated signaling pathways were regulated by miR-483, including transforming growth factor-β signaling, Wnt signaling and inflammatory response, cell adhesion, response to hypoxia, apoptotic processes, oxidative reduction processes and negative regulation of cell migration and proliferation.
2020-03-16 | GSE146774 | GEO
Project description:miRNA abnormalities are increasingly relevent to cancer development, We used microarrays to detail the global programme of gene expression upon miR-483 overexpression in sarcoma cell line MHH-ES-1. MHH-ES-1 cells were transfected with miR-483-5p, -3p or scrambled control mimics and then harvested 48 hours after to isolate total RNAs using Trizol reagent (Invitrogen). Total RNA was converted to cRNA probes using the BioArray High Yield Transcript Labeling Kit (ENZO diagnostics), and hybridized to Affymetrix GeneChip human HG-U133ver2+ 3’-mRNA expression microarray chips using protocol EukGEs2v4 on the GeneChip Fluidic Station.
2013-12-31 | E-GEOD-50980 | biostudies-arrayexpress
Project description:miR-483 overexpression in human sarcoma cell line MHH-ES-1.
| PRJNA219469 | ENA
Project description:Impact of miR-199-5p, miR-199a-3p and miR-214-3p overexpression on human lung fibroblasts
| PRJNA382975 | ENA
Project description:Colorectal cancer is a prevalent disease that is the third most common cause of cancer-associated death globally. The genetic mechanisms underlying tumor aggressiveness in colorectal cancer require further elucidation. Taking advantage of a large panel of human metastatic colorectal cancer xenografts and matched stem-like cell cultures (m-colospheres), we show here that overexpression of miRNA-483-3p, encoded by a frequently amplified gene locus encompassing IGF2, confers an aggressive phenotype. Following ectopic overexpression of miRNA-483-3p, m-colospheres displayed (i) increased proliferative response to exogenous EGFR family ligands EGF and neuregulin 1; (ii) increased spontaneous and growth factor-induced invasiveness and epithelial-mesenchymal transition (EMT); and (iii) enhanced stem-cell frequency and resistance to differentiation. Transcriptomic analyses and functional validation found that miRNA-483-3p directly targets NDRG1, a known metastasis suppressor responsible for downregulation of the EGFR family. As a result, induced or endogenous miRNA-483-3p overexpression associated with stimulation of the signaling pathway triggered by ERBB3, including AKT and GSK3β, which is responsible for EMT transcription factor activation. Consistently, treatment of miRNA-483-3p-overexpressing m-colospheres with selective ERBB3 antibodies counteracted their proliferative and invasive phenotype. The pro-malignant role of miRNA-483-3p was further corroborated by analysis of human colorectal tumors, where miRNA-483-3p expression levels directly correlated with expression of EMT transcription factors and poor prognosis, and downregulation of miRNA-483-3p, which prevented invasion of tumors formed by m-colosphere transplantation. These results unveil a previously unrecognized link between miRNA-483-3p, NDRG1, and ERBB3-AKT signaling, which can directly support colorectal cancer invasion and is amenable to therapeutic targeting.
2023-03-13 | GSE209535 | GEO
Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.
2019-08-12 | PXD014988 | Pride
Project description:Background: Adrenal myelolipoma (AML) is a relatively common and invariably benign tumor composed of adipose tissue and hematopoietic elements. Due to the variable proportion of fat and hematopoietic elements, it is sometimes challenging to differentiate AML from adrenocortical carcinoma (ACC). MicroRNAs have been identified as promising biomarkers in many tumors, including adrenocortical neoplasms, but the microRNA expression of adrenal myelolipoma has not been investigated, yet. Aims: To perform a large scale microRNA expression profiling in adrenal myelolipoma, benign and malignant adrenocortical tumors to identify potential microRNA biomarkers. Methods: Next-generation sequencing (NGS) on 30 formalin-fixed paraffin-embedded archived tissue samples (discovery cohort: 10 adrenocortical adenoma (ACA), 10 ACC and 10 myelolipoma) was performed by Illumina MiSeq. Significantly differentially expressed microRNAs were validated by real-time RT-qPCR in an independent validation cohort comprised of 10 ACA, 10 myelolipoma and 9 ACC samples. Results: We have found relative overexpression of miR- 451a, miR-486-5p, miR-363-3p and miR-150-5p in myelolipoma compared to the other two tumor groups by NGS. For ACC, we have found up-regulation of miR-184, miR-483-5p, miR-431-5p and miR-183-5p compared to myelolipoma and ACA. Validation by RT-qPCR, confirmed significant overexpression of miR-451a, miR-486-5p and miR-150-5p in myelolipomas relative to ACA and ACC, whereas significant overexpression of miR-184 and miR-183-5p was confirmed in ACC relative to the other 2 groups. The overexpression of miR-483-5p has not turned out to be significant in ACC relative to myelolipomas in the validation cohort. Conclusions: Overexpressed miR-451a, miR-486-5p and miR-150-5p might be potential tissue markers of adrenal myelolipoma. The lack of significance in the expression of miR-483-5p between ACC and myelolipoma is remarkable, as miR-483-5p has been considered to be the best marker of adrenal malignancy to date.
2018-04-07 | GSE112804 | GEO
Project description:miR-129-3p control cilia assembly by regulating CP110 and actin dynamics [miR-129-3p overexpression]
| PRJNA150147 | ENA
Project description:In 2019, our group performed small RNA-sequencing on keratinocytes isolated from lesional and non-lesional psoriasis skin as well as from healthy skin, and identified miRNAs with altered levels in psoriasis keratinocytes (Srivastava et al., 2019). One of the miRNAs we identified to be overexpressed in psoriasis keratinocytes was miR-378a-3p. In this study, we aimed to explore the regulation and function of miR-378a in keratinocytes and its potential role in psoriasis. We used microarrays to identify differentially expressed genes upon miR-378a overexpression in primary human keratinocytes as part of the study and gain insights about the modulation of specific pathways.
2021-03-08 | GSE164400 | GEO