Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma [RNA-seq]

ABSTRACT: The goal is to profile cFos binding sites in an p53 knockout mouse bone marrow-derived stem cells (mBMSCs).

ORGANISM(S): Mus musculus

PROVIDER: GSE89014 | GEO | 2017/08/11

SECONDARY ACCESSION(S): PRJNA349803

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma [ChIP-seq]

Project description:The goal is to profile cFos binding sites in an p53 knockout mouse bone marrow-derived stem cells (mBMSCs).

2017-08-11 | GSE88986 | GEO

cFOS-SOX9 Axis Reprograms Bone Marrow-Derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma.

Project description:Bone marrow-derived mesenchymal stem cells (BMSCs) are proposed as the cells of origin of several subtypes of osteosarcoma (OS). However, signals that direct BMSCs to form different subtypes of OS are unclear. Here we show that the default tumor type from spontaneously transformed p53 knockout (p53_KO) BMSCs is osteoblastic OS. The development of this default tumor type caused by p53 loss can be overridden by various oncogenic signals: RAS reprograms p53_KO BMSCs into undifferentiated sarcoma, AKT enhances osteoblastic OS, while cFOS promotes chondroblastic OS formation. We focus on studying the mechanism of cFOS-induced chondroblastic OS formation. Integrated genome-wide studies reveal a regulatory mechanism whereby cFOS binds to the promoter of a key chondroblastic transcription factor, Sox9, and induces its transcription in BMSCs. Importantly, SOX9 mediates cFOS-induced cartilage formation in chondroblastic OS. In summary, oncogenes determine tumor types derived from BMSCs, and the cFOS-SOX9 axis is critical for chondroblastic OS formation.

| S-EPMC5470112 | biostudies-literature

cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-08-11 | GSE89015 | GEO

cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma

Project description:cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma

| PRJNA349798 | ENA

Toxoplasma and Eimeria co-opt the host cFos expression for intracellular development in mammalian cells

Project description:Successful asexual reproduction of intracellular pathogens depend on their potential to exploit host resources and subvert antimicrobial defense. Here, we deployed two prevalent intracellular parasites of mammalian cells, namely Toxoplasma gondii and Eimeria falciformis, to identify the potential host determinants of infection. Expression analyses of the young adult mouse colonic (YAMC) epithelial cells showed regulation of several distinct transcripts upon infection by either parasite, indicating that closely-related pathogens program their intracellular niches in notably adaptive manner. Conversely, parasitized mouse embryonic fibroblasts (MEFs) exhibited a divergent transcriptome compared to corresponding YAMC cells, suggesting that individual host cells mount fairly discrete response while encountering a given pathogen. Among a limited set of factors similarly regulated by both parasites, we identified cFos, a master transcription factor, that was consistently induced throughout infection. Indeed, the asexual development of T. gondii and E. falciformis was severely impaired in MEF cells lacking cFos expression. Last but not least, our comparative transcriptomics of the parasitized MEFs (wild-type and cFos-/- mutant) and YAMC epithelial cells disclosed a cFos-network, underlying signal transduction cascades, as well as a repertoire of nucleotides-binding and ion-binding proteins, which are likely co-opted by coccidian pathogens to acclimatize the mammalian host environment.

2021-01-27 | GSE157395 | GEO

Genome wide mapping for TF binding sites for Pol II, JunD, cFos, Max & cMyc in GM12878 (ENCODE Project)

Project description:We performed ChIP-Seq for 5 different transcription factors (Pol II, JunD, cFos, Max and cMyc) as part of the ENCODE project in order to determine sites of allele-specific binding. This was done in the GM12878 cell line which was genotyped as part of the pilot II phase of the 1000 genomes project. There is a matching RNA-Seq experiemnt performed on the same cell line. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Mapping TF binding sites for 5 different TFs to assess allele-specific binding

2011-07-09 | E-GEOD-30399 | biostudies-arrayexpress

CircNRIP1 Encapsulated by Bone Marrow Mesenchymal Stem Cell-Derived Extracellular Vesicles Aggravates Osteosarcoma by Modulating the miR-532-3p/AKT3/PI3K/AKT Axis.

Project description:Emerging evidence indicates that extracellular vesicle (EV)-encapsulated circRNAs have the potential diagnostic and prognostic values for malignancies. However, the role of circNRIP1 in osteosarcoma remains unclear. We herein investigated the therapeutic potential of circNRIP1 delivered by bone marrow mesenchymal stem cell-derived EVs (BMSC-EVs) in osteosarcoma. The expression of circNRIP1 was examined in the clinical tissue samples of osteosarcoma patients, after which the downstream genes of circNRIP1 were bioinformatically predicted. Gain- and loss-of function assays were then performed in osteosarcoma cells with manipulation of circNRIP1 and miR-532-3p expression. EVs isolated from BMSCs were characterized and co-cultured with osteosarcoma cells to examine their effects on cell phenotypes, as reflected by CCK-8 and Transwell assays. Further, a mouse model of tumor xenografts was established for in vivo substantiation. circNRIP1 was upregulated in osteosarcoma tissues and cells. Overexpression of circNRIP1 promoted the proliferative, migratory, and invasive potential of osteosarcoma cells. Co-culture data showed that BMSC-EVs could transfer circNRIP1 into osteosarcoma cells where it competitively bound to miR-532-3p and weakened miR-532-3p's binding ability to AKT3. By this mechanism, the PI3K/AKT signaling pathway was activated and the malignant characteristics of osteosarcoma cells were stimulated. In vivo experimental results unveiled that circNRIP1-overexpressing BMSC-EVs in nude mice resulted in enhanced tumor growth. In conclusion, the BMSC-EV-enclosed circNRIP1 revealed a new molecular mechanism in the pathogenesis of osteosarcoma, which might provide a novel therapeutic target for osteosarcoma.

| S-EPMC8511523 | biostudies-literature

bZIP dimers CREB1, ATF2, Zta, ATF3|cJun, and cFos|cJun prefer binding some DNA sequences containing 5-formylcytosine and 5-carboxylcytosine

Project description:In mammalian cells, 5-methylcytosine (5mC) occurs in genomic double-stranded DNA (dsDNA) and is enzymatically oxidized to 5-hydroxymethylcytosine (5hmC), then to 5-formylcytosine (5fC), and finally to 5-carboxylcytosine (5caC). These cytosine modifications are enriched in regulatory regions of the genome. The effect of these oxidative products on five bZIP dimers (CREB1, ATF2, Zta, ATF3|cJun, and cFos|cJun) binding to five types of dsDNA was measured using protein binding microarrays. The five dsDNAs contain either cytosine in both DNA strands or cytosine in one strand and either 5mC, 5hmC, 5fC, or 5caC in the second strand. Some sequences containing the CEBP half-site GCAA are bound more strongly by all five bZIP domains when dsDNA contains 5mC, 5hmC, or 5fC. dsDNA containing 5caC in some TRE (AP-1)-like sequences, e.g., TGACTAA, is better bound by Zta, ATF3|cJun, and cFos|cJun.

2020-11-16 | GSE141050 | GEO

Genome wide mapping for TF binding sites for Pol II, JunD, cFos, Max & cMyc in GM12878 (ENCODE Project)

2011-07-09 | GSE30399 | GEO

Regeneration of hyaline-like cartilage in situ with SOX9 stimulation of bone marrow-derived mesenchymal stem cells.

Project description:Microfracture, a common procedure for treatment of cartilage injury, induces fibrocartilage repair by recruiting bone marrow derived mesenchymal stem cells (MSC) to the site of cartilage injury. However, fibrocartilage is inferior biomechanically to hyaline cartilage. SRY-type high-mobility group box-9 (SOX9) is a master regulator of chondrogenesis by promoting proliferation and differentiation of MSC into chondrocytes. In this study we aimed to test the therapeutic potential of cell penetrating recombinant SOX9 protein in regeneration of hyaline cartilage in situ at the site of cartilage injury. We generated a recombinant SOX9 protein which was fused with super positively charged green fluorescence protein (GFP) (scSOX9) to facilitate cell penetration. scSOX9 was able to induce chondrogenesis of bone marrow derived MSC in vitro. In a rabbit cartilage injury model, scSOX9 in combination with microfracture significantly improved quality of repaired cartilage as shown by macroscopic appearance. Histological analysis revealed that the reparative tissue induced by microfracture with scSOX9 had features of hyaline cartilage; and collagen type II to type I ratio was similar to that in normal cartilage. This short term in vivo study demonstrated that when administered at the site of microfracture, scSOX9 was able to induce reparative tissue with features of hyaline cartilage.

| S-EPMC5493350 | biostudies-literature

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