Expression data from NDRG1 depleted SKBR3 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE112841 | GEO | 2018/06/21
REPOSITORIES: GEO
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Project description:expression data from NDRG1 depleted SKBR3 cells
| PRJNA449286 | ENA
Project description:N-myc downstream-regulated gene 1 (*NDRG1*) is induced by cellular stress such as hypoxia and DNA damage, and in humans, germ line mutations cause Charcot-Marie-Tooth disease. However, the roles of NDRG1 in the cell are not fully understood. Previously, NDRG1 was shown to mediate doxorubicin resistance under hypoxia, suggesting a role for NDRG1 in cell survival under these conditions. We found decreased apoptosis in doxorubicin-treated cells expressing NDRG1 shRNAs under normoxia, demonstrating a requirement for NDRG1 in apoptosis in breast epithelial cells under normal oxygen pressure. We further compared expression profiles in human breast epithelial cells ectopically over-expressing NDRG1 with cells expressing NDRG1 shRNAs in order to identify biological pathways where NDRG1 is involved. The results suggest that NDRG1 may have roles connected to vesicle transport. The previously reported roles of NDRG1 in apoptosis, myelin sheet maintenance, enhanced exocytosis in mast cells and in cellular responses to hypoxia, heavy metals, and androgen may all converge by NDRG1 having a role linked to vesicle transport.
2011-11-04 | GSE33437 | GEO
Project description:Host cells harbor various intrinsic mechanisms to restrict viral infections as a first line of antiviral defense. Viruses have evolved various countermeasures against these antiviral mechanisms. Here we show that N-Myc Downstream-Reguated Gene 1 (NDRG1) limits productive HCV infection by inhibiting viral assembly. Interestingly, HCV infection down-regulates NDRG1 protein and mRNA expression. Loss of NDRG1 increases the size and number of lipid droplets, which are the sites of HCV assembly. HCV suppresses NDRG1 expression by up-regulating MYC, which directly inhibits the transcription of NDRG1. Up-regulation of MYC also leads to reduced expression of NDRG1-specific kinase SGK1, resulting in markedly diminished phosphorylation of NDRG1. Knockdown of MYC during HCV infection rescues NDRG1 expression and phosphorylation, suggesting that MYC regulates NDRG1 at both transcriptional and post-translational levels. Overall, our results suggest that NDRG1 restricts HCV assembly by limiting lipid droplet formation. HCV counteracts this intrinsic antiviral mechanism by down-regulating NDRG1 via a MYC-dependent mechanism.
2017-11-17 | GSE106988 | GEO
Project description:N-myc downstream-regulated gene 1 (*NDRG1*) is induced by cellular stress such as hypoxia and DNA damage, and in humans, germ line mutations cause Charcot-Marie-Tooth disease. However, the roles of NDRG1 in the cell are not fully understood. Previously, NDRG1 was shown to mediate doxorubicin resistance under hypoxia, suggesting a role for NDRG1 in cell survival under these conditions. We found decreased apoptosis in doxorubicin-treated cells expressing NDRG1 shRNAs under normoxia, demonstrating a requirement for NDRG1 in apoptosis in breast epithelial cells under normal oxygen pressure. We further compared expression profiles in human breast epithelial cells ectopically over-expressing NDRG1 with cells expressing NDRG1 shRNAs in order to identify biological pathways where NDRG1 is involved. The results suggest that NDRG1 may have roles connected to vesicle transport. The previously reported roles of NDRG1 in apoptosis, myelin sheet maintenance, enhanced exocytosis in mast cells and in cellular responses to hypoxia, heavy metals, and androgen may all converge by NDRG1 having a role linked to vesicle transport. SUM102 and ME16C2 stably transduced with siRNA against NDRG1 compared with empty vector control ZR-75-1 stably transduced with NDRG1 overexpression construct compared with empty vector control Two condition design
2011-11-04 | E-GEOD-33437 | biostudies-arrayexpress
Project description:Fasting triggers diverse physiological adaptations including increases in circulating fatty acids and mitochondrial respiration to facilitate organismal survival. The mechanisms driving mitochondrial adaptations and respiratory sufficiency during fasting remain incompletely understood. Here we show that fasting or lipid availability stimulates mTORC2 activity. Activation of mTORC2 and phosphorylation of its downstream target NDRG1 at Ser336 sustains mitochondrial fission and respiratory sufficiency. Timelapse imaging shows that NDRG1, but not phosphorylation-deficient NDRG1Ser336Ala mutant, engages with mitochondria to facilitate fission in both control and Drp1-deficient cells, reflecting independency from Drp1. Using proteomics, an siRNA screen, and epistasis experiments, we show that mTORC2-phosphorylated NDRG1 cooperates with small GTPase Cdc42 and effectors and regulators of Cdc42 to orchestrate fission. Accordingly, RictorKO, NDRG1Ser336Ala mutants, and Cdc42-deficient cells each display mitochondrial phenotypes reminiscent of fission failure. During nutrient surplus, mTOR complexes perform anabolic functions; however, paradoxical reactivation of mTORC2 during fasting unexpectedly drives mitochondrial fission and respiration.
2023-04-27 | PXD041696 | Pride
Project description:NDRG1 functions as a metastasis suppressor in pancreatic and other cancers. To determine the molecular function of NDRG1 in MIAPaCa-2 pancreatic cancer cells, we performed a whole genome gene array analysis on these cells stably transfected with NDRG1 when compared to empty vector-transfected controls. The differentially expressed genes indetified in this microarray may represent potential molecular targets of NDRG1 in pancreatic cancer.
2011-07-23 | GSE25086 | GEO
Project description:NDRG1 functions as a metastasis suppressor in pancreatic and other cancers. To determine the molecular function of NDRG1 in MIAPaCa-2 pancreatic cancer cells, we performed a whole genome gene array analysis on these cells stably transfected with NDRG1 when compared to empty vector-transfected controls. The differentially expressed genes indetified in this microarray may represent potential molecular targets of NDRG1 in pancreatic cancer. Two separate RNA extracts of MIAPaCa-2 vector control and NDRG1 transfected cells were collected and hybridised to Affymetrix Human Genome U133 Plus 2.0 chips.
2011-07-22 | E-GEOD-25086 | biostudies-arrayexpress
Project description:To investigate the target gene of lncRNA NDRG1-OT1 in breast cancer
2017-12-31 | GSE72881 | GEO
Project description:We sought to identify changes in placental gene expression that may contribute to the phenotype of NDRG1-deficient embryos, and to define the contribution of hypoxia and fetal sex to these changes. We therefore used high-density oligonucleotide microarrays to interrogate differences in placental gene expression, stratified by fetal sex, Ndrg1 status (WT vs KO) and oxygenation (21% vs 12%). C57Bl6/J mice heterozygous for NDRG1-null allele were bred and separated next day (E0.5), and give ad libitum access to standard chow and water with 12h light:dark cycle. Pregnant dams were sacrificed at E15.5 by cervical dislocation following isoflurane anesthesia. Following sacrifice, embryos and placentas were collected, NDRG1 genotype and sex were determined by PCR of fetal tissue, and RNA was extracted from placental tissue following removal of membranes.
2013-04-26 | E-GEOD-46381 | biostudies-arrayexpress
Project description:We sought to identify changes in placental gene expression that may contribute to the phenotype of NDRG1-deficient embryos, and to define the contribution of hypoxia and fetal sex to these changes. We therefore used high-density oligonucleotide microarrays to interrogate differences in placental gene expression, stratified by fetal sex, Ndrg1 status (WT vs KO) and oxygenation (21% vs 12%).
2013-04-26 | GSE46381 | GEO