Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5929673_1.fastq.gz | Fastqsanger.gz | |||
| SRR5929673_2.fastq.gz | Fastqsanger.gz | |||
| SRR5929683.fastq.gz | Fastqsanger.gz | |||
| SRR5929674_1.fastq.gz | Fastqsanger.gz | |||
| SRR5929674_2.fastq.gz | Fastqsanger.gz |
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Project description:To determine the physiological roles of NCOA4 and NCOA4-mediated ferritinophagy in hippocampal neurons, NCOA4 was depleted using siRNA and desferrioxamine (DFO; 100 µM, 24 h) was added to restrict iron availability. Cells were treated for NCOA4 depletion, iron restriction, or both, and then the transcriptome profiles acquired from RNA-seq were compared with those of control (scramble siRNA-treated) cells.
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Project description:Purpose: Knocking down NCOA4 disrupted Thyroid hormone receptor beta agonist,GC-1, mediated terminal human erythroblast differentiation. Therefore, we conducted RNA-seq to profile the transcriptome changes in NCOA4 knocked down human erythroblasts.. Methods: Human CD34+ cells were transduced by lentiviruses encoding shRNAs targeting either LacZ (control) or NCOA4 atday 1 of culture. At day 14, cells were switched to terminal differentiation medium. Results: Using an optimized data analysis workflow, we have identified an ensemble of genes whose expression are discrupted by NCOA4 knockdown. Conclusions: There is a significant correlation between the degree of GC-1-mediated gene activation and the degree of NCOA4 knockdown-mediated gene repression.
2017-09-06 | GSE102582 | GEO
Project description:To determine the physiological roles of NCOA4 and ferritinophagy in macrophages, NCOA4 was depleted via liposome-mediated siRNA delivery into cells. Cells were treated with siRNA for NCOA4 depletion and then the transcriptome profiles acquired from RNA-seq were compared with those of control (scramble siRNA-treated) cells.
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Project description:NCOA4 ChIP-seq on human K562 For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2019-03-03 | GSE127414 | GEO
Project description:Oncogenic KRAS rewires pancreatic ductal adenocarcinoma (PDAC) metabolism to promote dependence on autophagy and iron metabolism. NCOA4-mediated ferritinophagy links autophagy and iron metabolism as NCOA4 selectively targets ferritin, the cellular iron storage complex, via autophagy to the lysosome for ferritin degradation and release of iron for utilization. Using patient-derived and genetically engineered murine models of PDAC we now demonstrate that ferritinophagy is upregulated in PDAC to sustain iron availability thereby promoting PDAC progression. PDAC global quantitative proteomics reveals that ferritinophagy fuels iron-sulfur cluster synthesis to support mitochondrial homeostasis. Targeting NCOA4 leads to tumor growth delay and prolonged survival but with development of compensatory iron acquisition pathways. Finally, a ferritinophagy gain-of-function PDAC murine model demonstrates worse survival, and an elevated ferritinophagy expression signature predicts for worse overall survival in human PDAC patients. Together, our data define NCOA4-mediated ferritinophagy as a therapeutic target in PDAC and reveal that maintenance of cellular iron homeostasis is a critical cell autonomous function of PDAC autophagy.
2022-08-17 | PXD033356 | Pride
Project description:Treatment with thyroid hormone receptor beta agonist, GC-1, significantly increased the signal intensities of the top 300 NCOA4 chromatin binding sites, which overlapped with binding sites for Pol II as well as with histone marks associated with active transcription, such as H3K27Ac and H3K4Me3, but not with marks such as H3K4Me1 commonly associated with enhancers
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Project description:Acute myeloid leukemia (AML) remains a challenging hematological malignancy with poor prognosis and limited treatment options. Post-therapy relapse, particularly driven by leukemic stem cells (LSCs), contributes to therapeutic failure and adverse outcome. Here, we investigated the role of quiescence and its associated molecular mechanisms in AML pathogenesis and identified potential vulnerabilities for therapeutic intervention. We found that quiescent AML cells, enriched for LSC functions, exhibited a distinct gene set that served as a significant prognostic factor for poor outcomes in AML patients. Furthermore, quiescent cells displayed heightened autophagic activity, with a reliance on ferritinophagy, a selective form of autophagy mediated by Nuclear Receptor Coactivator 4 (NCOA4), for iron bioavailability. Inhibition of NCOA4 genetically or chemically showed potent anti-leukemic effects, particularly targeting the LSC compartment. These findings uncover that ferritinophagy inhibition may represent a promising therapeutic strategy for patients with AML.
2024-06-16 | GSE235060 | GEO
Project description:Acute myeloid leukemia (AML) remains a challenging hematological malignancy with poor prognosis and limited treatment options. Post-therapy relapse, particularly driven by leukemic stem cells (LSCs), contributes to therapeutic failure and adverse outcome. Here, we investigated the role of quiescence and its associated molecular mechanisms in AML pathogenesis and identified potential vulnerabilities for therapeutic intervention. We found that quiescent AML cells, enriched for LSC functions, exhibited a distinct gene set that served as a significant prognostic factor for poor outcomes in AML patients. Furthermore, quiescent cells displayed heightened autophagic activity, with a reliance on ferritinophagy, a selective form of autophagy mediated by Nuclear Receptor Coactivator 4 (NCOA4), for iron bioavailability. Inhibition of NCOA4 genetically or chemically showed potent anti-leukemic effects, particularly targeting the LSC compartment. These findings uncover that ferritinophagy inhibition may represent a promising therapeutic strategy for patients with AML.
2024-06-16 | GSE235058 | GEO
Project description:Acute myeloid leukemia (AML) remains a challenging hematological malignancy with poor prognosis and limited treatment options. Post-therapy relapse, particularly driven by leukemic stem cells (LSCs), contributes to therapeutic failure and adverse outcome. Here, we investigated the role of quiescence and its associated molecular mechanisms in AML pathogenesis and identified potential vulnerabilities for therapeutic intervention. We found that quiescent AML cells, enriched for LSC functions, exhibited a distinct gene set that served as a significant prognostic factor for poor outcomes in AML patients. Furthermore, quiescent cells displayed heightened autophagic activity, with a reliance on ferritinophagy, a selective form of autophagy mediated by Nuclear Receptor Coactivator 4 (NCOA4), for iron bioavailability. Inhibition of NCOA4 genetically or chemically showed potent anti-leukemic effects, particularly targeting the LSC compartment. These findings uncover that ferritinophagy inhibition may represent a promising therapeutic strategy for patients with AML.
2024-06-16 | GSE235069 | GEO
Project description:Acute myeloid leukemia (AML) remains a challenging hematological malignancy with poor prognosis and limited treatment options. Post-therapy relapse, particularly driven by leukemic stem cells (LSCs), contributes to therapeutic failure and adverse outcome. Here, we investigated the role of quiescence and its associated molecular mechanisms in AML pathogenesis and identified potential vulnerabilities for therapeutic intervention. We found that quiescent AML cells, enriched for LSC functions, exhibited a distinct gene set that served as a significant prognostic factor for poor outcomes in AML patients. Furthermore, quiescent cells displayed heightened autophagic activity, with a reliance on ferritinophagy, a selective form of autophagy mediated by Nuclear Receptor Coactivator 4 (NCOA4), for iron bioavailability. Inhibition of NCOA4 genetically or chemically showed potent anti-leukemic effects, particularly targeting the LSC compartment. These findings uncover that ferritinophagy inhibition may represent a promising therapeutic strategy for patients with AML.
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