Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

USP29 coordinates MYC and HIF1α stabilization to promote tumor metabolism and progression

ABSTRACT: Deleption of USP29 significantly inhibits aerobic glycolysis, glutamine catabolism and proliferation of cancer cells. To test the underlying mechanisms, RNA-seq was performed using USP29 or control depleted SK-N-BE2 and Ramos cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE180797 | GEO | 2021/10/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

USP29-mediated HIF1a stabilization promotes Sorafenib resistance of hepatocellular carcinoma cells by upregulating glycolysis

Project description:Understanding the mechanisms underlying evasive resistance in cancer is an unmet medical need to improve the efficacy of current therapies. In hepatocellular carcinoma (HCC), aberrant expression of hypoxia inducible factor 1 a (HIF1a) and increased aerobic glycolysis metabolism represent drivers of the development of resistance to therapy with the multi-kinase inhibitor Sorafenib. However, it has remained unknown how HIF1a is activated and how its activity and the subsequent induction of aerobic glycolysis promotes Sorafenib resistance in HCC. Here, we report the ubiquitin-specific peptidase USP29 as a new regulator of HIF1a and of aerobic glycolysis during the development of Sorafenib resistance in HCC. In particular, we have identified USP29 as a critical deubiquitylase (DUB) of HIF1a, which directly deubiquitinates and stabilizes HIF1a and, thus, promotes its transcriptional activity. Among the transcriptional targets of HIF1a is the gene encoding for hexokinase 2 (HK2), a key enzyme of the glycolytic pathway. The absence of USP29, and thus of HIF1a transcriptional activity, reduces the levels of aerobic glycolysis and reinstalls the sensitivity to Sorafenib treatment in Sorafenib-resistant HCC cells in vitro and in xenograft transplantation mouse models in vivo. Notably, the absence of USP29 and high HK2 expression levels correlate with the response of HCC patients to Sorafenib therapy. Together, the data demonstrate that, as a DUB of HIF1a, USP29 promotes Sorafenib resistance in HCC cells by upregulating glycolysis, thereby opening new avenues for therapeutically targeting Sorafenib-resistant HCC in patients.

2021-07-27 | GSE158458 | GEO

USP29 coordinates MYC and HIF1α stabilization to promote tumor metabolism and progression

Project description:USP29 coordinates MYC and HIF1α stabilization to promote tumor metabolism and progression

| PRJNA749584 | ENA

Homo sapiens

Project description:miR-34 regulates JARID1A expresion (SK-N-BE2)

| PRJNA215103 | ENA

Time-resolved phosphoproteomic analysis of ZIKV-infected cells

Project description:To investigate cellular pathway dysregulation upon ZIKV infection, time-resolved phosphoproteomics LC-MS/MS analysis was used. ZIKV-infected SK-N-BE2 cells or mock-treated cells were harvested 24, 48 and 72 hours post virus infection and their phosphoproteome was quantitatively analyzed by label-free LC-MS/MS.

2018-09-03 | PXD009560 | Pride

HIF1α stabilization in hypoxia is not oxidant-initiated.

Project description: Not available

| S-EPMC8530508 | biostudies-literature

Global Interactome of ZIKV (FSS13025) viral proteins.

Project description:To identify the global cellular interactome of each ZIKV proteins, individual HA-tagged ZIKV proteins (FSS13025 Asian strain) were expressed in the neuroblastoma cell line SK-N-BE2 using lentivirus-mediated delivery. Cellular lysates were subjected to Affinity purification (AP) using HA-agarose beads, and eluates digested with Trypsin and LysC before analysis via LC-MS/MS using an Orbitrap instrument.

2018-09-03 | PXD009551 | Pride

miR-34 regulates JARID1A expresion (SK-N-BE2)

Project description:p53 inactivation occurs only rarely in neuroblastoma, although miR-34, a transcriptional target of p53, is often deleted in neuroblastoma, suggesting another way in which p53 signaling might be impaired. In this study we show that miR-34 directly targets and downregulates the Polycomb Repressive Complex 2 (PRC2) and its associated histone demethylase, JARID1A, in a p53-dependent manner, 4 samples were transfected with miRNA control or miR-34a, miR-34b, miR-34c into SK-N-BE2 cells.

2014-01-01 | E-GEOD-49845 | biostudies-arrayexpress

Deubiquitinase USP29 Ameliorates Pathological Cardiac Hypertrophy Through Inhibiting TAK1

Project description:The identification of key factors involved in pathological cardiac hypertrophy is crucial to exploring novel treatments for heart failure. In this study, we elucidated the role of Ubiquitin-specific protease 29 (USP29), a deubiquitinase, in pressure overload-induced cardiac hypertrophy. Genetic knockout of USP29 in mice significantly exacerbated TAC-induced heart hypertrophy, dysfunction, and fibrosis; whereas overexpression of USP29 in cardiomyocytes attenuated the hypertrophic response. Similarly, USP29 markedly alleviated PE-induced hypertrophy of primary neonatal rat cardiomyocytes. Mechanistically, the cardio-protective effects mediated by USP29 were attributed to its suppression of transforming growth factor β-activated kinase 1 (TAK1)-JNK/P38 signaling pathway activation. Collectively, our study suggests that targeting either USP29 or its interaction with TAK1 could represent an innovative therapeutic strategy for treating heart failure and cardiac hypertrophy.

2024-04-20 | GSE263965 | GEO

Be1 and Be2 B cells are transcriptionally distinct

Project description:B cells cultured in the presence of Th1 CD4 T cells (Be1) or Th2 CD4 T cells (Be2) lead to distinct phenotypic outcomes. To determine when the phenotypic differences emerged, IgD positive and IgD negative Be1 and Be2 cells were isolated from cultures derived from 3 independent donors and RNA-seq performed. These data define the transcriptional differences of Be1 and Be2 cells ad distinct differentiation stages and show that Be1 B cells contain a pre-ASC signature that is absent from Be2 B cells.

2019-05-17 | GSE95282 | GEO

Extended ZIKV-NS4B interactome (AP-MS/MS analysis of ZIKV interacting proteins)

Project description:To identify the cellular interactors of ZIKV-NS4B-interacting proteins and their differential composition upon ZIKV infection, individual cDNAs expressing FLAG-tagged variants of the following ZIKV-NS4B-interacting proteins were generated (GeneBank and UniProt Accession numbers are given in parenthesis): CEND1 (BC034732.1; Q8N111), CHP1 (BC031293; Q99653), CLN6 (BC010849.1; Q9NWW5), TMEM41b (BC035034.1; Q5BJD5), RBFOX2 (NM_001082579.1; O43251-6), BSG (BC009040.2;P35613). Lentiviruses expressing each of these proteins were used to transduce SK-N-BE2 cells, which were either mock-infected or infected with ZIKV (H/PF/2013, MOI=3), and 72 hours later subjected to AP-MS/MS to identify the respective cellular interactors.

2018-09-03 | PXD009561 | Pride

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