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Differentially regulated genes in control and c-myc N-myc deficient LT-HSCs

ABSTRACT: Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs. LT-HSC (Lin-Sca1+CD150+CD48-) cells were sorted from the BM of MxCre c-myc flox2 N-myc flox2 (experimental) and c-myc flox2 N-myc flox2 (control) mice 3 days after the last pI-pC injection. Each condition was analysed in triplicates, with each replicate consisting of a pool of 3 dKO mice or 2 control mice.

ORGANISM(S): Mus musculus

SUBMITTER: Elisa Laurenti

PROVIDER: E-GEOD-12467 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Hematopoietic stem cell function and survival depend on c-Myc and N-Myc activity.

Laurenti Elisa E Varnum-Finney Barbara B Wilson Anne A Ferrero Isabel I Blanco-Bose William E WE Ehninger Armin A Knoepfler Paul S PS Cheng Pei-Feng PF MacDonald H Robson HR Eisenman Robert N RN Bernstein Irwin D ID Trumpp Andreas A

Cell stem cell 20081201 6

Myc activity is emerging as a key element in acquisition and maintenance of stem cell properties. We have previously shown that c-Myc deficiency results in accumulation of defective hematopoietic stem cells (HSCs) due to niche-dependent differentiation defects. Here we report that immature HSCs coexpress c-myc and N-myc mRNA at similar levels. Although conditional deletion of N-myc in the bone marrow does not affect hematopoiesis, combined deficiency of c-Myc and N-Myc (dKO) results in pancytope ...[more]

PMID: 19041778

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Differentially regulated genes in control and c-myc N-myc deficient progenitors

Project description:Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs and commited progenitors.

2009-02-20 | GSE12536 | GEO

Differentially regulated genes in control and c-myc N-myc deficient LT-HSCs

2009-02-20 | GSE12467 | GEO

IFNa activates dormant HSCs in vivo

Project description:Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. Upon injury these cells are induced to proliferate in order to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNα), HSCs efficiently exit G0 and enter an active cell cycle. HSCs respond to IFNα treatment by increased phosphorylation of STAT1 and PKB/Akt, expression of IFNα target genes and up-regulation of stem cell antigen-1 (Sca-1). HSCs lacking either the interferon-α/β receptor (IFNAR), STAT1 or Sca-1 are insensitive to IFNα stimulation, demonstrating that STAT1 and Sca-1 mediate IFNα induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-FU1, HSCs pre-treated (primed) with IFNα and thus induced to proliferate are efficiently eliminated by 5-FU exposure in vivo. Conversely, HSCs chronically activated by IFNα are functionally compromised and are rapidly out competed by non-activatable IFNAR-/- cells in competitive repopulation assays. In summary, while chronic activation of the IFNα pathway in HSCs impairs their function, acute IFNα treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNα on leukemic cells and raise the possibility for novel applications of type I interferons to target cancer stem cells. cDNA microarray analysis was performed on sorted Lin neg, cKit+, CD150+, CD48neg HSCs from IFNα treated (16h after treatment) and untreated (littermate) mice. Per condition 3 independent biological replicates were analysed.

2009-01-15 | E-GEOD-14361 | biostudies-arrayexpress

Ectopic Myc expression

Project description:Ectopic Myc Expression in P493-6 B-cells at three levels: High Myc, Low Myc and No Myc High Myc, Low Myc and No Myc expressions

2010-03-09 | E-GEOD-19703 | biostudies-arrayexpress

Gene expression data from Medicago truncatula mutant plantlet roots treated with Myc-LCOs.

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2012-05-30 | E-GEOD-33637 | biostudies-arrayexpress

EZH2 depletion potentiates MYC degradation inhibiting neuroblastoma and small cell carcinoma tumor formation

Project description:Efforts to therapeutically target EZH2 have generally focused on inhibition of its methyltransferase activity, although it remains less clear whether this is the central mechanism whereby EZH2 promotes cancer. We demonstrate that EZH2 directly interacts with both MYC family oncoproteins, MYC and MYCN, and promotes their stabilization in a methyltransferase-independent manner. By competing against the SCFFBW7 ubiquitin ligase to bind MYC and MYCN, EZH2 counteracted FBW7-mediated MYC(N) polyubiquitination and proteasomal degradation. Depletion, but not enzymatic inhibition, of EZH2 induced robust MYC(N) degradation and inhibited tumor cell growth in MYC(N) driven neuroblastoma and small cell lung cancer. These findings unveil the MYC family proteins as global EZH2 oncogenic effectors and EZH2 pharmacologic degraders as potential MYC(N) targeted cancer therapeutics, pointing out that MYC(N) driven cancers may develop inherent resistance to the canonical EZH2 enzymatic inhibitors currently in clinical development.

2022-02-17 | PXD029652 | Pride

Genome-wide characterization of the transcriptional program of Myc-dependent transformation

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2009-11-24 | E-GEOD-14264 | biostudies-arrayexpress

mRNA expression data from BCR-ABL, MYC and CD22DE12 transgenic mouse models

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2015-06-25 | E-GEOD-58872 | biostudies-arrayexpress

Role of c-Myc haploinsufficiency in the maintenance of HSCs

Project description:Role of c-Myc haploinsufficiency in the maintenance of HSCs

| PRJNA657604 | ENA

Bone morphogenetic protein-7 is a MYC target with pro-survival functions in childhood medulloblastoma

Project description:Medulloblastoma (MB) is the most common malignant brain tumor in children, among whom overexpression or amplification of MYC oncogenes has been associated with poor clinical outcome. Although the MYC functions during normal development and oncogenesis in various systems have been extensively investigated, the transcriptional targets mediating MYC effects in MB are still elusive. Their identification and roles during MB onset and progression are important and will ultimately suggest novel potential therapeutic targets. cDNA microarray analysis was used to compare the effects of overexpressing and silencing MYC on the transcriptome of a MB-derived cell line. We identified 209 genes with potential relevance to MYC-dependent cellular responses in MB. Among the MYC-responsive genes, we found members of the bone morphogenetic protein (BMP) signaling pathway, which plays a crucial role during the development of the cerebellum. In particular, the cytokine gene BMP7 was identified as a direct target of MYC in MB cells. Similar to the effect induced by BMP7 silencing by siRNA, the use of a small-molecule inhibitor of the BMP/SMAD signaling pathway reduced cell viability in a panel of MB cells. Altogether, our findings indicate that high MYC levels drive BMP7 expression in MB to induce pro-survival and pro-proliferative cellular pathways. This observation suggests that targeting the BMP/SMAD pathway may be a new therapeutic concept for the treatment of childhood MB. 6 samples (3 replicates for each sample): wild-type MB cell line, empty vector-transfected control cell line, 2 c-MYC-overexpressing clones, 1 clone upon c-MYC silencing, 1 silencing control cell line.

2011-05-16 | E-GEOD-22139 | biostudies-arrayexpress

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