Genome-wide transcriptome profile in response to expression of ectopic MYC proteins [RNA-seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE102917 | GEO | 2018/08/20
REPOSITORIES: GEO
Similar Datasets
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
Project description:Ectopic Myc Expression in P493-6 B-cells at three levels: High Myc, Low Myc and No Myc
2010-02-25 | GSE19703 | GEO
Project description:Targeted depletion of ribosomal protein S6 (Rps6) from hepatoblasts of the developing liver results in neonatal sub-lethal hepatic failure due to inhibition of bile duct development and widespread induction of hepatocyte death triggering regeneration. Overexpression of c-Myc is hepatoprotective in the context of Rps6-deficiency and eliminates the need for DS6 livers to regenerate by preventing hepatocyte death. Microarrays were used to identify the transcriptional program associated with loss of hepatic Rps6 and to identify mRNAs associated with c-Myc's hepatoprotective effect in DS6 livers
2023-01-04 | GSE212363 | GEO
Project description:C-MYC (henceforth MYC) is one of the most frequently overexpressed oncogenes in human cancer and even modestly deregulated MYC expression can initiate ectopic proliferation in many post-mitotic, terminally differentiated cell types in vivo. Metazoan organisms have consequently evolved a number of mechanisms to counteract MYC's oncogenic potential, of which apoptosis is arguably the best understood. However, the mechanisms through which MYC induces apoptosis remains controversial, with some studies implicating p19ARF-mediated stabilization of p53, followed by induction of pro-apoptotic BH3 family member NOXA and PUMA, while others argue for more direct regulation of BH3 proteins, especially BIM. The debate likely stems from the use of different experimental systems, modes of perturbation, and quite possibly different levels of MYC expression. Here, we use a single experimental system to systematically evaluate the roles of p19ARF and BIM during MYC-induced apoptosis, in vitro, in vivo, and in combination with a widely used tumoricidal chemotherapeutic, Doxorubicin. We find a common specific requirement for BIM during MYC-induced apoptosis in multiple settings, which does not extend to the p53-responsive BH3 family member PUMA, and find no evidence of a role for p19ARF during MYC-induced apoptosis in the tissues examined. MYC-ER ChIP-Seq with HC20 anti-ER antibody in MCF10A cells performed on an Illumina IIx Genome Analyzer.
2015-05-18 | E-GEOD-59001 | biostudies-arrayexpress
Project description:Multiple myeloma (MM) is a malignant plasma cell disorder and frequently characterized by the 16 dysregulation of the MYC oncogene, which is associated with poor prognosis and disease progression. While MYC's involvement in transcriptional regulation is well-established, the functional role of MYC target proteins and the impact on post-transcriptional processes in MM cells remain poorly understood. This study employed Stable Isotope Labeling with Amino Acids in Cell Culture (SILAC) coupled with mass spectrometry analysis to investigate the effects of MYC depletion on the proteome of MM cells. The results revealed that MYC primarily regulates translational processes. Specifically, the three RNA-binding proteins (RBPs) 4EBP1, hnRNPC, and LARP1, were prominently down-regulated upon MYC depletion in MM cells. Notably, high expression levels of these proteins were correlated with poor survival and disease progression in MM patients. These findings highlight the critical role of MYC in the regulation of translation and identify 4EBP1, hnRNPC, and LARP1 as MYC target proteins. Targeting these proteins may offer new therapeutic strategies and prognostic markers for MM, potentially improving patient outcomes. This study provides valuable insights into the post-transcriptional regulatory mechanisms mediated by MYC and opens avenues for further research in understanding and treating this devastating disease.
2023-06-15 | MSV000092169 | MassIVE
Project description:Tumor necrosis factor (TNF) receptor-associated factor (TRAF)-interacting protein (TRAIP), a RING domain-containing E3 ligase, has emerged as a key player in safeguarding genome integrity and is closely linked to cancer. Here, we discovered that TRAIP exhibits low expression in bladder cancer (BLCA), which correlates with poor prognosis. TRAIP exerts inhibitory effects on bladder cancer cell proliferation and migration both in vitro and in vivo. MYC serves as a newly identified target for TRAIP, with direct interaction leading to the promotion of K48 polyubiquitination at K428/430 lysine residues, subsequently resulting in proteasome-dependent degradation and downregulation of MYC's transcriptional activity. This process effectively hinders the progression of bladder cancer. Restoration of MYC expression rescues the suppressed proliferation and migration of bladder cancer cells induced by TRAIP. Furthermore, our investigation also demonstrates that MYC binds to the transcriptional start region of TRAIP, exerting regulatory control over TRAIP transcription. Consequently, this interaction establishes a negative feedback loop that prevents excessive expression of MYC. In summary, our study uncovers a novel mechanism by which TRAIP inhibits the progression of bladder cancer through the ubiquitinated degradation of MYC.
2023-12-28 | GSE237002 | GEO
Project description:C-MYC (henceforth MYC) is one of the most frequently overexpressed oncogenes in human cancer and even modestly deregulated MYC expression can initiate ectopic proliferation in many post-mitotic, terminally differentiated cell types in vivo. Metazoan organisms have consequently evolved a number of mechanisms to counteract MYC's oncogenic potential, of which apoptosis is arguably the best understood. However, the mechanisms through which MYC induces apoptosis remains controversial, with some studies implicating p19ARF-mediated stabilization of p53, followed by induction of pro-apoptotic BH3 family member NOXA and PUMA, while others argue for more direct regulation of BH3 proteins, especially BIM. The debate likely stems from the use of different experimental systems, modes of perturbation, and quite possibly different levels of MYC expression. Here, we use a single experimental system to systematically evaluate the roles of p19ARF and BIM during MYC-induced apoptosis, in vitro, in vivo, and in combination with a widely used tumoricidal chemotherapeutic, Doxorubicin. We find a common specific requirement for BIM during MYC-induced apoptosis in multiple settings, which does not extend to the p53-responsive BH3 family member PUMA, and find no evidence of a role for p19ARF during MYC-induced apoptosis in the tissues examined.
2015-05-18 | GSE59001 | GEO
Project description:The functions of key oncogenic transcription factors independent of context have not been fully delineated despite our richer understanding of the genetic alterations in human cancers. The MYC oncogene, which produces the Myc transcription factor, is frequently altered in human cancer and is a major regulatory hub for many cancers. In this regard, we sought to unravel the primordial signature of Myc function by using high-throughput genomic approaches to identify the cell-type independent core Myc target gene signature. Using a model of human B lymphoma cells bearing inducible MYC, we identified a stringent set of direct Myc target genes via chromatin immunoprecipitation (ChIP), global nuclear run-on assay, and changes in mRNA levels. We also identified direct Myc targets in human embryonic stem cells (ESCs). We further document that a Myc core signature (MCS) set of target genes is shared in mouse and human ESCs as well as in four other human cancer cell types. Remarkably, the expression of the MCS correlates with MYC expression in a cell-type independent manner across 8,129 microarray samples, which include 312 cell and tissue types. Furthermore, the expression of the MCS is elevated in vivo in Em-Myc transgenic murine lymphoma cells as compared with premalignant or normal B lymphocytes. Expression of the MCS in human B cell lymphomas, acute leukemia, lung cancers or Ewing sarcomas has the highest correlation with MYC expression. Annotation of this gene signature reveals Myc's primordial function in RNA processing, ribosome biogenesis and biomass accumulation as its key roles in cancer and stem cells. This SuperSeries is composed of the SubSeries listed below.
2011-09-19 | GSE32220 | GEO
Project description:To identify proteomic signatures associated with hepatocellular carcinoma driven by MYC overexpression, proteomics was performed on the LAP-tTA/tetO-MYC mouse conditional liver cancer model. Upon MYC activation, mice form liver cancer. Differential proteomics was performed in "MYC on" (MYC-HCC) mouse liver tumors versus mouse control normal liver tissue (where MYC was not overexpressed to drive tumorigenesis -- "MYC off").
2022-10-12 | PXD031478 | Pride
Project description:Mechanisitc model of PI3K and ERK signal integration by Myc. ERK and PI3K regulated Myc satbility by phosphorylating the same. (PMID:18463697)
2024-09-02 | BIOMD0000000818 | BioModels