Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiR-7977 transfer alter the transcriptome in bone marrow mesenchymal stem cells.

ABSTRACT: Acute myeloid leukemia (AML) cells release abundant exosomal miR-7977 that transfer into bone marrow (BM) mesenchymal stromal cells (MSCs). We have shown that exosomal miR-7977 was highly released from AML cells and was transferred into BM MSCs. It has been well known that a microRNA has multiple targets. In fact, miRDB predicted 633 targets. Based on these findings, control and miR-7977mimic were transferred into BM MSCs. Subsequently, alteration of transcriptome was analyzed to gain insight into the role of miR-7977 in bone marrow micro environment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE108186 | GEO | 2019/03/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data in bone marrow mesenchymal stromal cells derived from acute myeloid leukemia patients

Project description:Acute myeloid leukemia (AML) is a heterogeneous clonal disorder of hematopoietic stem/progenitor cells characterized by excessive proliferation and subsequent accumulation of immature myeloid blasts, leading to impaired hematopoiesis in the bone marrow (BM). The progression of AML is closely linked to the crosstalk between leukemic cells and the BM microenvironment, in particular the mesenchymal stromal cells (MSCs). We compared the mRNA expression profile of BM-MSCs from newly diagnosed AML patients (n=3), relapsed AML patients (n=3) and healthy donor controls (n=3)

2021-11-26 | GSE122917 | GEO

mRAN expression profiles in bone marrow mesenchymal stem cells (MSC) from Wild Type and Lama4-deficient mice co-cultured with MLL-AF9 AML cells

Project description:Bone marrow (BM) niche contributes to hematopoietic regeneration and can be remodeled by leukemic cells. We have found that Lama4 deletion in mouse mesenchymal stem cells (MSCs) could promote the proliferation of MLL-AF9 acute myeloid leukemia (AML) cells and chemoresistance of the cells to chemotherapy cytarabine. However, whether Lama4 deficient MSCs are more susseptible for AML cell remodeling remains to be explored. Here we report that differential molecular alterations in Lama4 deficient MSCs compared to wild type MSCs after being exposed to the AML cells for 48hours, which might be related to the enhanced AML cell proliferation and chemoresistance.

2022-02-16 | GSE185846 | GEO

Roles of hsa-miR-12462 and SLC9A1 in acute myeloid leukemia

Project description:In this study, we defined a novel miRNA, hsa-miR-12462, through small RNA sequencing of the bone marrow (BM) cells from 128 newly diagnosed subjects with AML

2020-08-22 | GSE156654 | GEO

Bone marrow stromal cells induce an ALDH+ stem cell-like phenotype and enhance chemotherapy resistance in AML cells through a TGF-β-p38-ALDH2 pathway

Project description:Our study aims to examine the interaction between AML cells and other cells in the tumor microenvironment, specifically bone marrow derived mesenchymal stromal cells. To delineate the specific genes/pathways involved in this interaction, we have co-cultured AML cell lines alone or with bone marrow derived mesenchymal stromal cells for 3 days, extracted total RNA from AML cells and analyzed the samples by RNA-seq. We identified the genes that are differentially expressed in co-cultured AML cells compared to AML cells alone. We found that TGF-β1 associated gene signature is activated in AML cells in the presence of BM-MSCs compared to AML cells alone.

2020-06-23 | GSE152996 | GEO

Molecular profiling of Ebf2+ and Ebf2- PαS mesenchymal stem cells from mouse dorsal skin

Project description:While extensive efforts have been on understanding bone marrow (BM) niche contribution to normal and malignant hematopoiesis, the role of extramedullary niches has been largely ignored. Evidence suggests a BM mesenchymal stem cell (MSC) counterpart exists in skin. However, their native identity and role in hematopoiesis remain unexplored. Here, we demonstrated that mouse skin harbors MSC subsets that are phenotypically and molecularly similar to BM MSCs, including a primitive MSC population marked by Early B-cell Factor 2 (Ebf2) and downstream MSCs lacking Ebf2. Functionally, skin MSCs not only support acute myeloid leukemia (AML) stem cells but also protect them from chemotherapy. This persistence of AML cells in skin were further amplified in AML-promoting microenvironment lacking Lama4. Our study demonstrated the features of extramedullary niches in skin and their previously unrecognized role in supporting AML stem cells during chemotherapy, opening a new path for understanding the extramedullary manifestation of AML in patients.

2023-07-16 | GSE167562 | GEO

Comparison of bone-marrow mesenchymal stromal cells from multiple myeloma patients and healthy donors

Project description:It is now well established that bone marrow (BM) constitutes a microenvironment required for differentiation. Bone marrow mesenchymal stromal cells (BM-MSCs) strongly support MM cell growth, by producing a high level of Interleukin-6 (IL-6), a major MM cell growth factor. BM-MSCs also support osteoclastogenesis and angiogenesis. Previous studies have suggested that the direct (VLA-4, VCAM-1, CD44, VLA-5, LFA-1, syndecan-1,…) and indirect interactions (soluble factors) between MM plasma cells and BM-MSCs result in constitutive abnormalities in BM-MSCs. In particular, MM BM-MSCs express less CD106 and fibronectin and more DKK1, IL-1β and TNF-α as compared with normal BM-MSCs. In order to gain a global view of the differences between BM-MSCs from MM patients and healthy donors, we used gene expression profiling to identify genes associated to the transformation of MM BM-MSCs.

2013-03-21 | GSE36474 | GEO

Effect of PROTAC-mediated BRD4 degradation on bone marrow-derived mesenchymal stromal cells [BM-MSCs]

Project description:BRD4, a member of the BET family of histone readers, binds to acetylated lysine of histone H3 and promotes assembly of super-enhancer complexes that drive expression of key oncogenes in acute myeloid leukemia (AML) and other cancers. ARV-825 is a proteolysis-targeting chimera (PROTAC) that targets BRD4 for CRBN-mediated ubiquitination and degradation. BM-MSCs are an important element of the bone marrow microenvironment of AML. To understand how targeting BRD4 in BM-MSCs may contribute to the overall effect on AML of targeting BRD4, we treated BM-MSCs from two normal donors with ARV-825 in vitro. Treatment of BM-MSC monocultures with ARV-825 for 24 hr caused extensive changes in gene expression, highly uniform between triplicates. Although the cultures from the two normal donors showed different profiles, their changes with ARV-825 were highly similar. These changes implicated effects on oxidative stress, osteogenic differentiation, retinoid metabolism, F-actin polymerization, CXCL12, and proliferation.

2019-10-01 | GSE101449 | GEO

miR-146a-5p expression effect on human mesenchymal stem cell

Project description:Analysis of human mesenchymal stem cells (MSC) from bone marrow and the Wharton's jelly of the umbilical cord after manupulating miR-146a-5p expression. miR-146a-5p is involved in controlling the proliferation and migration of MSCs. Results provide miR-146a-5p-regulating genes in MSCs. In this study, BM-MSCs transduced with miR-146a-5p expression vector or pCDH-CMV-MCS-EF1-copGFP vector only, as well as two WJ-MSCs transfected with short interfering RNAs targeting miR-146a or a GFP control.

2013-09-05 | E-GEOD-44186 | biostudies-arrayexpress

Development of gene expression signatures for mesenchymal stem cells from neuroblastoma patients

Project description:To obtain genetic evidence about the interaction between MSCs and metastatic NB cancer cells in bone marrow (BM), we isolated bone marrow-derived MSCs from children with NB and compared their global expression patterns with MSCs obtained from normal pediatric donors using the Agilent 44K microarrays.

2012-07-01 | GSE35133 | GEO

Expression data from porcine mandibular- and tibial-derived bone marrow mesenchymal stem cells.

Project description:Objective: Craniofacial bone defects caused by injuries and congenital diseases are a formidable challenge to clinicians. Research has shown promise in using bone marrow mesenchymal stem cells (BM-MSCs) from limb bones for craniofacial bone regeneration; yet little is known about the potential of BM-MSCs from craniofacial bones. This study compared BM-MSCs isolated from limb and craniofacial bones in pigs, a preclinical model closely resembling humans. Design: Bone marrow was aspirated from the tibia and mandible of four-month-old pigs (n=4), followed by BM-MSC isolation, culture-expansion and confirmation by flow cytometry. Proliferation rates were compared using population doubling times. Osteogenic differentiation was evaluated by quantifying alkaline phosphatase (ALP) activity. Total mRNA was extracted from freshly isolated BM-MSCs and analyzed to compare gene expressions of tibial and mandibular BM-MSCs using an Affymetrix GeneChip porcine genome array, followed by real-time RT-PCR evaluation of two neural crest markers. Results: BM-MSCs from both locations expressed MSC markers without expression of hematopoietic markers. Mandibular BM-MSCs proliferated significantly faster than tibial BM-MSCs. Without osteogenic inducers, mandibular BM-MSC alkaline phosphatase activities were 3.3-fold greater than those of tibial origin. Microarray analysis identified 383 differentially expressed genes in mandibular and tibial BM-MSCs, including higher expression of cranial neural crest-related genes nestin and BMP-4 in mandibular BM-MSCs, a trend also confirmed by real-time RT-PCR. Among differently expressed genes, only 47 showed greater than 1.5-fold differences in expression. Conclusions: These data indicate that despite many similarities in gene expression, mandibular BM-MSCs express of number of genes differently than tibial BM-MSCs and have a phenotypic profile that may make them advantageous for craniofacial bone regeneration.

2016-05-14 | GSE81430 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data