Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA396177 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MicroRNAs are important cellular regulators and their dysfunctions are associated with various disease. miR-371/372/373 was found co-regulated in HBV-producing HepG2.2.15 cells when compared to its non-HBV producing maternal HepG2 cells. To obtain a glimpse of the potential influence of the enforced miR-371-372-373 cluster in HepG2 gene expression, a two-color Capitalbio 70-mer oligo microarray platform, which contained 21,329 well-characterized human gene probes, was used to identify the differentially expressed genes between miR-371-372-373-HepG2 and mock-HepG2 in two independent biological replicate. miR-371-372-373-HepG2 vs. mock-HepG2
2012-01-15 | E-GEOD-19981 | biostudies-arrayexpress
Project description:MicroRNAs are important cellular regulators and their dysfunctions are associated with various disease. miR-371/372/373 was found co-regulated in HBV-producing HepG2.2.15 cells when compared to its non-HBV producing maternal HepG2 cells. To obtain a glimpse of the potential influence of the enforced miR-371-372-373 cluster in HepG2 gene expression, a two-color Capitalbio 70-mer oligo microarray platform, which contained 21,329 well-characterized human gene probes, was used to identify the differentially expressed genes between miR-371-372-373-HepG2 and mock-HepG2 in two independent biological replicate.
2012-01-15 | GSE19981 | GEO
Project description:The miR-371~373 cluster is a suspected repressor of colon cancer initiation and progression. To better understand its role in metastasis initiation, we used microarray expression analysis to identify potential target genes of this miRNA cluster Potential target genes were defined as significantly downregulated genes after stable overexpression of the miR-371~373 cluster
2018-07-23 | GSE102001 | GEO
Project description:Malignant testicular germ cells tumors (TGCTs) are the most common solid cancers in young men. Current TGCT diagnostics include conventional serum protein markers, but these lack the sensitivity and specificity to serve as accurate markers across all TGCT subtypes. MicroRNAs (miRNAs) are small non-coding regulatory RNAs and informative biomarkers for several diseases. In humans, miRNAs of the miR-371-373 cluster are detectable in the serum of patients with malignant TGCTs and outperform existing serum protein markers for both initial diagnosis and subsequent disease monitoring. We previously developed a genetically engineered mouse model featuring malignant mixed TGCTs consisting of pluripotent embryonal carcinoma (EC) and differentiated teratoma that, like the corresponding human malignancies, originate in utero and are highly chemosensitive. Here, we report that miRNAs in the mouse miR-290-295 cluster, homologs of the human miR-371-373 cluster, were detectable in serum from mice with malignant TGCTs but not from tumor-free control mice or mice with benign teratomas. miR-291-293 were expressed and secreted specifically by pluripotent EC cells, and expression was lost following differentiation induced by the drug thioridazine. Notably, miR-291-293 levels were significantly higher in the serum of pregnant dams carrying tumor-bearing fetuses compared to that of control dams. These findings reveal that expression of the miR-290-295 and miR-371-373 clusters in mice and humans, respectively, is a conserved feature of malignant TGCTs, further validating the mouse model as representative of the human disease. These data also highlight the potential of serum miR-371-373 assays to improve patient outcomes through early TGCT detection, possibly even prenatally.
2025-02-12 | GSE260949 | GEO
Project description:Naïve human pluripotent stem cells (hPSC) represent an earlier time-point in embryogenesis than conventional, ‘primed’ hPSCs. We present a comprehensive miRNA profiling of naïve-to-primed transition in hPSC, a process resembling aspects of early in vivo embryogenesis. We identify miR-143-3p and miR-22-3p as markers of the naïve state and miR-363-5p, several members of the miR-17 family, miR-302 family as primed markers. We uncover that miR-371-373 are highly upregulated in naïve hPSC. MiR-371-373 are the human homologs of the mouse miR-290 family, which are the most highly expressed miRNAs in mPSC. This aligns with the consensus that naïve hPSC resemble mPSC, showing that the absence of miR-371-373 in conventional hPSC is due to cell state rather than a species difference.
2020-06-29 | GSE128260 | GEO
Project description:Background. MiR-371~373 and miR-302/367 cluster over-expression occurs in all malignant- GCTs, regardless of age (paediatric/adult), site (gonadal/extragonadal), or subtype [seminoma, yolk sac tumour (YST), embryonal carcinoma (EC)]. Six of eight microRNAs from these clusters contain the seed ‘AAGUGC’, determining mRNA targeting. Here we sought to identify the significance of these observations by targeting these microRNAs functionally. Methods. We targeted miR-371~373 and/or miR-302/367 clusters in malignant-GCT cell lines, using CRISPR-Cas9, gapmer primary miR-302/367 transcripts inhibition, and peptide- nucleic-acid (PNA) or locked-nucleic-acid (LNA)-DNA inhibition targeting miR-302a-d-3p, and undertook relevant functional assays. Results. MiR-302/367 cluster microRNAs made the largest contribution to AAGUGC seed abundance in malignant-GCT cells, regardless of subtype (seminoma/YST/EC). Following unsuccessful use of CRISPR-Cas9, gapmer, and PNA systems, LNA-DNA-based targeting resulted in growth inhibition in seminoma and YST cells. This was associated with de- repression of multiple mRNAs targeted by ‘AAGUGC’ seed-containing microRNAs, with pathway analysis confirming predominant disruption of Rho-GTPase signaling, vesicle organization/transport, and cell-cycle regulation, findings corroborated in clinical samples. Further LNA-DNA inhibitor studies confirmed direct cell-cycle effects, with increase of cells in G0/G1-phase and decrease in S-phase. Conclusion. Targeting of specific miR-371~373 and miR-302/367 microRNAs in malignant- GCTs demonstrated their functional significance, with growth inhibition mediated through cell-cycle disruption.
2024-08-01 | E-MTAB-13323 | biostudies-arrayexpress
Project description:Malignant germ-cell-tumours (GCTs) are characterised by microRNA (miRNA/miR-) dysregulation, with universal over-expression of miR-371~373 and miR-302/367 clusters regardless of patient age, tumour site, or subtype (seminoma/yolk-sac-tumour/embryonal carcinoma). These miRNAs are released into the bloodstream, presumed within extracellular-vesicles (EVs) and represent promising biomarkers. Here, we comprehensively examined the role of EVs, and their miRNA cargo, on (fibroblast/endothelial/macrophage) cells representative of the testicular GCT (TGCT) tumour microenvironment (TME). Small RNA next-generation-sequencing was performed on 34 samples, comprising representative malignant GCT cell lines/EVs and controls (testis fibroblast [Hs1.Tes] cell-line/EVs and testis/ovary samples). TME cells received TGCT co-culture, TGCT-derived EVs, and a miRNA overexpression system (miR-371a-OE) to assess functional relevance. TGCT cells secreted EVs into culture media. MiR-371~373 and miR-302/367 cluster miRNAs were overexpressed in all TGCT cells/subtypes compared with control cells and were highly abundant in TGCT-derived EVs, with miR-371a-3p/miR-371a-5p the most abundant. TGCT co-culture resulted in increased levels of miRNAs from the miR-371~373 and miR-302/367 clusters in TME (fibroblast) cells. Next, fluorescent labelling demonstrated TGCT-derived EVs were internalised by all TME (fibroblast/endothelial/macrophage) cells. TME (fibroblast/endothelial) cell treatment with EVs derived from different TGCT subtypes resulted in increased miR-371~373 and miR-302/367 miRNA levels, and other generic (eg, miR-205-5p/miR-148-3p) and subtype-specific (seminoma, eg, miR-203a-3p; yolk-sac-tumour, eg, miR-375-3p) miRNAs. MiR-371a-OE in TME cells resulted in increased collagen contraction (fibroblasts) and angiogenesis (endothelial cells), via direct mRNA downregulation and alteration of relevant pathways. TGCT cells communicate with nontumour stromal TME cells through release of EVs enriched in oncogenic miRNAs, potentially contributing to tumour progression.
2023-09-30 | E-MTAB-13322 | biostudies-arrayexpress
Project description:Background: Somatic-type malignancies (SM) arising in germ cell tumors (GCTs) represent aggressive and chemoresistant neoplasms frequently occurring as metastases after chemotherapy. Historically, SM have been interpreted as originating in teratoma; however, recent observations suggest that a subset may derive from yolk sac tumor. In this study, we evaluate the relationship between conventional histologic types of GCT and SM of germ cell origin by assessing expression of miR-371~373 and genomic methylation. Methods: A cohort of 97 samples (41 SM and 38 conventional GCTs, including paired conventional GCT and SMs from individual tumors) were assessed for miR-371~373 expression (RT-qPCR) and genomic DNA methylation (clinically validated assay). Results: Expression of miR-371~373 was higher in conventional non-teratomatous GCT than in SM (considered as a single category containing all histologic subtypes). However, miR-371~373 expression was heterogeneous among the latter, with significantly higher levels in sarcomatoid yolk sac tumor (SYST) and glandular neoplasms than in other SMs. Genomic DNA methylation analysis showed that SMs (considered as a single category) did not form a discrete cluster. Instead, they grouped into subclusters that intercalated with conventional GCTs. Analysis of paired conventional GCT and SM or “SM-like” components (i.e., components with SM histology that did not meet size criteria) from individual tumors demonstrated a clear separation according to histology, suggesting that epigenetic processes play a significant role in the transformation of GCT to SM. Discussion: A subset of SMs shows molecular similarities to (and may derive from) yolk sac tumor, with SYST and glandular yolk sac tumor possibly representing intermediate phenotypes. The transformation of conventional GCT into SM seems to be driven largely by epigenetic mechanisms, suggesting that trials of targeted treatment with epidrugs may be beneficial in selected patients.
2025-04-04 | GSE281147 | GEO
Project description:In this study, we used RNA sequencing to provide a comprehensive overview of the expression profiles of small non-coding transcripts carried by the extracellular vesicles (EVs) derived from human adipose tissue stromal/stem cells (AT-MSCs) and human pluripotent stem cells (hPSCs), both human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSC). Small non-coding RNA sequencing from EVs showed that the profile of miRNA expression in PSC follow the profile reported for cell derived miRNA; further, most abundant miRNAs were found to originate from specific miRNA families which are regulating pluripotency, reprograming and differentiation (miR-17–92, mir-200, miR-302/367, miR-371/373, CM19 microRNA cluster). For the AT-MSCs, the highly expressed miRNAs were found to be regulating osteogenesis (mir-let-7/98, miR-10/100, miR-125, miR-196, miR-199, miR-615-3p, mir-22-3p, mir-24-3p, mir-27a-3p, mir-193b-5p, mir-195-3p). Additionally, abundant small nuclear and nucleolar RNA were detected in PSCs, whereas Y- and tRNA were found in AT-MSCs. Identification of EV-miRNA and non-coding RNA signatures released by these stem cells will provide clues towards understanding their role in intracellular communications, and well as their roles in maintaining the stem cell niche.
2018-10-30 | GSE113868 | GEO
Project description:We report the generation and characterization of DICER1-deficient hESCs. We uncover an unexpected requirement for DICER1 as well as essential pro-survival roles of members of the mir-302- 367 and mir-371- 373 clusters in hESCs. Our work provides a robust platform for interrogating microRNA function in hESC and differentiation.
2018-08-01 | GSE113375 | GEO