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Genome-wide analysis of transformed MSCs

ABSTRACT: Analysis of transformed MSCs at gene expression level. The aim in the present study was that overexpression of MYC in the MSCs alter gene expression of MSCs. Results provide important information of the response of overexpresion of MYCs, such as up- or down-regulated specific anabolic/catabolic cellular functions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE25296 | GEO | 2011/10/10

SECONDARY ACCESSION(S): PRJNA134779

REPOSITORIES: GEO

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Genome-wide analysis of transformed MSCs

Project description:Analysis of transformed MSCs at gene expression level. The aim in the present study was that overexpression of MYC in the MSCs alter gene expression of MSCs. Results provide important information of the response of overexpresion of MYCs, such as up- or down-regulated specific anabolic/catabolic cellular functions. Total RNA obtained from transformed MSCs or MSC culture cells at different passages.

2011-10-09 | E-GEOD-25296 | biostudies-arrayexpress

Oncogene Regulated Release of Extracellular Vesicles

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Transcriptomic analysis of effect of oncolytic measles virus (MV) on transformed and non-transformed bone marrow-derived mesenchymal stem cells (MSCs)

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Differentially expressed genes between oncogene-transformed and non-transformed fetal liver progenitor cells

Project description:The activation of different oncogenic signals may primarily contribute to the heterogeneity of cancer cells. However, the exact mechanisms underlying different oncogenic transformation are still unclear. We used the c-Myc, H-Ras and Akt transformed liver cell model to define mRNA expression profiles in the non-transformed and the three types of oncogene-transformed cells Purified p53-/- mouse fetal liver progenitor cells were transformed by three oncogenic genetic factors, c-Myc, H-RasV12 and myristoylated-AKT1(myr-Akt). The gene expression profilings of transformed cells and control cells were analyzed through microarray.

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Oncogene regulated release of extracellular vesicles

Project description:Oncogenes reprogram multiple metabolic phenotypes of cancer cells including the balance between anabolic and catabolic processes, mechanisms of nutrient uptake, and choices in nutrient utilization. Here, we explore how different oncogenes regulate biomass loss via extracellular vesicle release. We use isogenic mammary breast epithelial cells transformed with a panel of oncogenes found commonly mutated, amplified or overexpressed in multiple cancers. We observe an increase in extracellular vesicle (EV) release upon oncogenic transformation, with MYC and AURKB oncogenes eliciting the highest number of EVs produced. Oncogene expression altered the protein composition of released EVs. Likewise, miRNAs were differentially sorted into EVs in an oncogene-specific manner. We performed an integrated pathway analysis of metabolites and gene expression across different oncogene-expressing cells and identified that ceramide-sphingosine metabolism was broadly deregulated, especially in MYC overexpressing cells. Inhibition of neutral sphingomyelinases (N-SMase) resulted in significant decrease in EV production in MYC high cells, while ESCRT-dependent small EV production predominated in AURKB cells.

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RNA sequence of ISL1-MSCs and Ctrl-MSCs

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Gene expression profile of c-MYC driven mouse liver tumours, compared with Normal livers from control mice

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Project description:Although different sarcomas have been modeled in mice upon expression of fusion oncogenes in MSCs, sarcomagenesis has not been successfully modeled in human MSCs (hMSCs). We report that FUS-CHOP, a hallmark fusion gene in mixoid liposarcoma (MLS), has an instructive role in lineage commitment, and its expression in hMSC sequentially immortalized/transformed with up to 5 oncogenic hits (p53 and Rb deficiency, hTERT over-expression, c-myc stabilization and H-RASv12 mutation) drives the formation of serially transplantable MLS. This is the first model of sarcoma based on the expression of a sarcoma-associated fusion protein in hMSC, and allowed us to unravel the differentiation processes and signaling pathways altered in the MLS-initiating cells. This study will contribute to test novel therapeutic approaches, and constitutes a proof-of-concept to employ hMSCs as target cell for modeling other fusion gene-associated human sarcomas.

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CUL3(BPM) E3 ubiquitin ligases regulate MYC2, MYC3 and MYC4 stability and JA responses

Project description:The Jasmonate pathway regulators MYC2, MYC3 and MYC4 are central nodes in plant signaling networks integrating environmental and developmental signals to fine-tune jasmonate defenses and plant growth. Hence, their activity needs to be tightly regulated in order to optimize plant fitness. Among the increasing number of mechanisms regulating MYCs, protein stability is arising as a major player. However, how the levels of MYCs proteins are modulated is still poorly understood. Here, we report that MYC2, MYC3 and MYC4 are targets of BPM proteins, which act as substrate adaptors of CUL3-based E3 ubiquitin ligases. Reduction-of-function of CUL3(BPM) in amiR-bpm lines, bpm235 triple mutants and cul3ab double mutants enhance MYC2 and MYC3 stability and accumulation, and potentiates plant responses to JA such a root-growth inhibition, and MYC-regulated gene expression. BPM3 protein is stabilized by JA, suggesting a new negative feedback regulatory mechanism to control MYCs activity. Our results uncover a new layer for JA-pathway regulation by CUL3(BPM)-mediated degradation of MYC TFs.

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