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To investigate the effects of NRF2 inhibitors (pyrimethamine and mitoxantrone) on gene expression in a human esophageal squamous cell carcinoma cell line (KYSE70)

ABSTRACT: To study the effects of NRF2 inhibitors (pyrimethamine or mitoxantrone) on human esophageal squamous cell carcinoma cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE173164 | GEO | 2024/04/22

REPOSITORIES: GEO

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To investigate the effects of NRF2 inhibitors (pyrimethamine and mitoxantrone) on mRNA expression in a human esophageal squamous cell carcinoma cell line (KYSE70 cells)

Project description:To study the effects of NRF2 inhibitors (pyrimethamine or mitoxantrone) on human esophageal squamous cell carcinoma cells.

2023-10-12 | GSE235587 | GEO

To investigate the effects of NRF2 inhibitors (pyrimethamine) on mRNA expression in mouse esophageal epithelium.

Project description:To study the effects of NRF2 inhibitors (pyrimethamine) on mRNA expression in mouse esophageal epithelium.

2023-10-12 | GSE235584 | GEO

Esophageal epithelium of 12 weeks old mice (WT, Nrf2-/-) on C57BL background with or without gastroesophageal reflux for 4 weeks.

Project description:Transcriptional profiling of adult esophageal epithelium comparing wild-type mice with Nrf2-/- mice with or without gastroesophageal reflux for 4 weeks. Goal was to determine the role of Nrf2 on the barrier function of mouse esophageal epithelium. Two-class comparisons. Wild-type/without reflux vs. Nrf2-/-/without reflux; Wild-type/gastric reflux vs. Nrf2-/-/gastric reflux; Wild-type/duodenal reflux vs. Nrf2-/-/duodenal reflux; Wild-type/mixed reflux vs. Nrf2-/-/mixed reflux. Biological replicates: 3 replicates for each group.

2013-01-01 | E-GEOD-39629 | biostudies-arrayexpress

Whole esophagi of WT, Nrf2-/- and Keap1-/- mice on C57BL background at E11.5, E15.5, P0 and P7, and esophageal epithelium of adult (8 weeks old) mice

Project description:Transcriptional profiling of mouse esophageal development. Goal was to globally profile critical genes and signaling pathways during the development of mouse esophagus and determine how Nrf2/Keap1 pathway regulates the morphogenesis of the esophageal epithelium. Mutiple-comparison. WT-E11.5 vs. WT-E15.5 vs. WT-P0 vs. WT-P7; WT-P7 vs. WT-adult; WT-adult vs. Nrf2-/--adult; WT-P7 vs. Nrf2-/--P7 vs. Keap1-/--P7 vs. Nrf2-/-Keap1-/--P7. Biological replicates: 3 replicates for each group.

2011-12-09 | E-GEOD-34278 | biostudies-arrayexpress

Esophageal epithelium of 12 weeks old mice (WT, Nrf2-/-) on C57BL background with or without gastroesophageal reflux for 4 weeks.

2013-01-01 | GSE39629 | GEO

Differential squamous cell fates elicited by NRF2 gain-of-function versus KEAP1 loss-of-function

Project description:Clinical evidence has revealed that high-level activation of NRF2 caused by somatic mutations in NRF2 is frequently detected in esophageal squamous cell carcinoma (ESCC), whereas that by somatic mutations in KEAP1, a negative regulator of NRF2, is not. Here, we challenged to generate a mouse model of NRF2-activated ESCC using the cancer-derived NRF2L30F mutation and cancer-driver mutant Trp53R172H. Concomitant expression of NRF2L30F and Trp53R172H induced proliferation of squamous cell epithelia and resulted in NRF2-activated ESCC-like lesions. In contrast, while squamous cell-specific deletion of KEAP1 induced similar NRF2 hyper-activation, the loss-of-KEAP1 combined with Trp53R172H did not elicit the proliferation and formation of ESCC-like lesions. Instead, KEAP1-deleted cells disappeared from the esophageal epithelium over time by cell competition. These findings provide insights into the observation that somatic mutations are more frequently observed in NRF2 than in KEAP1, and the mouse model developed here will be instrumental in elucidating the mechanistic basis leading to NRF2-activated ESCC.

2024-03-22 | GSE255927 | GEO

Whole esophagi of WT, Nrf2-/- and Keap1-/- mice on C57BL background at E11.5, E15.5, P0 and P7, and esophageal epithelium of adult (8 weeks old) mice

2011-12-09 | GSE34278 | GEO

African American esophageal squamous cell carcinoma expression profile reveals loss of detox networks

Project description:Esophageal carcinoma is the third most common gastrointestinal malignancy worldwide and is generally unresponsive to therapy. African Americans have an increased risk for esophageal squamous cell cancer (ESCC), the subtype that shows marked variation in geographic frequency. To identify key genes involved in ESC carcinogenesis in African Americans we conducted microarray expression profiling and found a significant dysregulation of genes encoding stress response and drug-metabolizing enzymes, mainly in NRF2 pathway. The involvement of NRF2 mediated oxidative damage represent a key step in the evolution of African American ESCC. Loss of activity of these enzymes would confer increased sensitivity of esophageal cells to xenobiotics, such as alcohol and tobacco smoke, and may account for the high incidence of ESCC in this ethnic group. The differential expression profile also indicates an inflammatory component and tissue regeneration in ESCC tumorigenesis. Together, these findings suggest a remarkable interplay of genetic and environmental factors in the pathogenesis of African American ESCC.

2017-08-15 | GSE77861 | GEO

Nrf2 ChIP-seq data of Nrf2KO, wild-type and Keap1KO esophagus

Project description:To understand how hyperactive NRF2 causes the esophageal phenotype in mice.

2018-11-15 | GSE122504 | GEO

Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus

Project description:NF-E2-related factor-2 (Nrf2) regulates the cellular response to oxidative/electrophilic stresses, and loss of Keap1 increases the Nrf2 protein level. As Keap1-null mice die of esophageal hyperkeratosis, whole-body phenotypes of Nrf2 hyperactivation in adult animals remain to be delineated. Here we show that deleting esophageal Nrf2 in Keap1-null mice the mice survive until adulthood, but develop polyuria with low osmolality and bilateral hydronephrosis. This novel phenotype is to be attributable to defects in water reabsorption caused by a reduction in the level of the aquaporin 2 (AQP2) channel in the kidney. In line, renal tubular deletion of Keap1 generates symptoms of nephrogenic diabetes insipidus, demonstrating that Nrf2 activation in developing tubular cells causes a water reabsorption defect. The rescue of mice from the lethal first hit of Keap1 ablation serves as a useful tool to study novel functions of Nrf2.

2017-06-12 | GSE84780 | GEO

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