Characterization of miRNomes in acute and chronic myeloid leukemia cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE48059 | GEO | 2014/07/03
SECONDARY ACCESSION(S): PRJNA208839
REPOSITORIES: GEO
Similar Datasets
Project description:An in-depth analysis of miRNomes in 3 human myeloid leukemia cell lines was carried out to comprehensively identify miRNAs that distinguish acute and chronic myeloid leukemias and relate to myeloid cell differentiation. Characterization the miRNomes in 3 myeloid leukemia cell lines.
2014-07-03 | E-GEOD-48059 | biostudies-arrayexpress
Project description:Chronic and acute myeloid leukemia (CML/AML) evade immune surveillance and induce immunosuppression, largely by upregulating Foxp3+ regulatory T cells (Treg). However, mechanisms that drive Treg in myeloid leukemias are largely unknown. Here, we show that leukemic (CML- and AML-derived) extracellular vesicles (EVs) drive human Treg, by de novo induction of Treg and by upregulating suppressive phenotype and activity of Treg. Rab27a-mediated EVs secretion contributed to Treg expansion, activity, and leukemic engraftment in vivo in a mouse model of CML-like disease. Leukemic EVs downregulated mTOR-S6 and upregulated STAT5 signaling in T cells, to upregulate Foxp3 and Treg activity, as well as evoked significant transcriptomic changes in Treg. By using high resolution 23-color spectral flow cytometry we identified 2 distinct, highly suppressive subsets of Treg expanded by leukemic EVs, characterized by elevated expression of tumor Treg markers CCR8, CCR4, TIGIT, CD39, CD30, TNFR2 and IL21R. Finally, we identified 4 1BBL/TNFSF9 protein in leukemic EVs. Deficiency of 4-1BBL in leukemic cells and EVs resulted in lower expression of CD30, TNFR2 and LAG-3 on Treg and thus weaker effector phenotype. Collectively, our data pinpoint leukemic extracellular vesicles as a significant factor that drives regulatory T cells and immunosuppression in myeloid leukemias. Our results suggest that targeting of Rab27a and EVs secretion may be a viable therapeutic option in myeloid leukemias, whereas detection of 4 1BBL containing EVs could be used as an early biomarker of immunosuppression and leukemia development/relapse
2022-02-16 | PXD027240 | Pride
Project description:Comparison of goat and cow milk-derived extracellular vesicle miRNomes (microRNA expression profiles) determined usiing RNA-sequencing (NGS).
2023-05-10 | GSE227559 | GEO
Project description: Not available
| S-EPMC4411353 | biostudies-literature
Project description:Effect of breed in mid lactation Holstein (H) and Montbéliarde (M) cows on mammary glande miRNA profile. Genetic polymorphisms are known to influence milk production and composition. However, genomic mechanisms involved in the genetic regulation of milk component synthesis are not completely understood. MicroRNAs (miRNA) regulate gene expression. The objective of the present study was to compare mammary gland miRNomes of two dairy cow breeds, Holstein and Montbéliarde, with different dairy performances. Milk, fat, protein, and lactose yields were lower in Montbéliarde than in Holstein cows. MiRNomes obtained using RNA-Seq technology from the mammary glands of Holstein (n = 5) and Montbéliarde (n = 6) lactating cows revealed 623 distinct expressed miRNAs, among which 596 were known and 27 were predicted miRNAs. The comparison of their abundance in the mammary gland of Holstein versus Montbéliarde cows showed 22 differentially expressed miRNAs (Padj ≤ 0.05). Among them, 11 presented a fold change ≥2, with 2 highly expressed miRNAs (miR-100 and miR-146b). Without taking into account the fold change, the differential miRNA with the highest abundance was miR-186, which is known to inhibit cell proliferation and epithelial-to-mesenchymal transition. Data mining showed that the 17 differentially expressed miRNAs with more than 20 reads on average, regulate mammary gland plasticity and may be related to the observed differences in milk production between Holstein and Montbéliarde, which are two breeds with different mammogenic potential. Some of the 17 miRNAs could potentially target mRNAs involved in signaling pathways (such as mTOR) and in lipid metabolism, thereby suggesting that they could influence milk composition. In conclusion, we showed differences in mammary gland miRNomes of two dairy bovine breeds. These differences suggest a potential role of miRNAs in mammary gland plasticity and in milk component synthesis related to milk production and composition.
2019-05-12 | GSE131057 | GEO
Project description:To comprehensively characterize the impact of TREM1 deficiency specifically within the tumor myeloid populations, we selectively enriched the CD45+CD11b+ tumor-infiltrating myeloid cells from tumor-bearing Trem1+/+ and Trem1-/- mice for scRNA-seq analysis.
2023-09-27 | E-MTAB-13246 | biostudies-arrayexpress
Project description:The concept of milk as a healthy food has opened the way for studies on milk components, from nutrients to microRNAs, molecules with broad regulatory properties present in large quantities in milk. Characterization of these components has been performed in several species, such as humans and bovine, depending on the stages of lactation. Here, we have studied the variation in milk microRNA composition according to genetic background. Using high throughput sequencing, we have characterized and compared the milk miRNomes of Holstein and Normande cattle, dairy breeds with distinct milk production features, in order to highlight microRNAs that are essential for regulation of the lactation process. In Holstein and Normande milk, 2,038 and 2,030 microRNAs were identified, respectively, with 1,771 common microRNAs, of which 1,049 were annotated and 722 were predicted. The comparison of the milk miRNomes of two breeds allowed to highlight 182 microRNAs displaying significant differences in the abundance. They are involved in the regulation of lipid metabolism and mammary morphogenesis and development, which affects lactation. Our results provide new insights into the regulation of molecular mechanisms involved in milk production.
2020-01-09 | GSE134670 | GEO
Project description:Objective: Bone marrow-derived myeloid cells accumulate in the liver as monocytes and macrophages during the progression of obesity-related non-alcoholic fatty liver disease (NAFLD) to steatohepatitis (NASH). Myeloid cells comprise heterogeneous subsets, and dietary overnutrition may affect macrophages in liver and bone marrow. We therefore aimed at characterizing in-depth the functional adaptations of myeloid cells in fatty liver. Design: We employed single-cell RNA-sequencing to comprehensively assess the heterogeneity of myeloid cells in liver and bone marrow during NAFLD, by analyzing C57BL/6 mice fed with a high-fat, high-sugar, high-cholesterol "Western diet" for 16 weeks. We also characterized NAFLD-driven functional adaptations of macrophages in vitro and their functional relevance during steatohepatitis in vivo.
2019-04-24 | GSE130180 | GEO
Project description:<p>Patients with myeloid malignancies bearing high-risk cytogenetic abnormalities lack effective therapies and have a poor overall survival. -7/del(7q) is identified in half of high-risk myeloid neoplasms. We recently identified <i>CUX1</i> to be a haploinsufficient myeloid tumor suppressor gene located within the commonly deleted segment of 7q22. Here we identify the spectrum of somatic mutations that co-occur with loss of <i>CUX1</i> and chromosome 7 in patients with <i>de novo</i> acute myeloid leukemia (AML) or a therapy-related myeloid neoplasm. -7/del(7q) leukemias have a distinct mutational profile characterized by low frequencies of alterations in major leukemogenic pathways, including genes encoding transcription factors, cohesin, and DNA-methylation-related proteins. In contrast, RAS pathway activating mutations occurred in 40% of -7/del(7q) samples, a significantly higher frequency than other AMLs and higher than previously reported. As targeted therapeutics advance, our data provide guidance for which pathways are most relevant in the treatment of adverse-risk myeloid leukemia. </p>
| phs000759 | dbGaP