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Loss of the Aryl Hydrocarbon Receptor (AhR) Promotes Cancer Cells Resistance to BRAFV600E Targeted Therapies. [RNA-Seq]

ABSTRACT: Loss of the Aryl Hydrocarbon Receptor (AhR) Promotes Cancer Cells Resistance to BRAFV600E Targeted Therapies. [RNA-Seq]

PROVIDER: PRJNA1207950 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31926738_1.fastq.gz	Fastqsanger.gz
	SRR31926738_2.fastq.gz	Fastqsanger.gz
	SRR31926739_1.fastq.gz	Fastqsanger.gz
	SRR31926739_2.fastq.gz	Fastqsanger.gz
	SRR31926740_1.fastq.gz	Fastqsanger.gz

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Loss of the Aryl Hydrocarbon Receptor (AhR) Promotes Cancer Cells Resistance to BRAFV600E Targeted Therapies. [CRISPR]

Project description:Predicting a patient’s response to chemotherapies and identifying additional molecular targets to improve treatment efficacy are major objectives in cancer research. BRAFV600E inhibitors targeting the MAP kinase pathway showed promising initial clinical results in thyroid cancers (TCs) for metastatic or recurrent tumors refractory to radioiodine treatments. BRAFV600E-targeted therapies have also been approved by the FDA for the treatment of some unresectable or metastatic BRAFV600E+ solid tumors. Still, for most patients, the response to BRAFV600E blocking therapy is transient due to cell proliferation reactivation through escape pathways. We performed a genome-wide CRISPR screen to reveal targets in TCs that facilitate resistance or sensitize thyroid cancer cells to inhibitors of the MAP kinase pathway. Among the genes that consistently altered MAPK inhibitor treatment response, we identified the Aryl hydrocarbon Receptor (AhR) and its molecular partner, the AhR nuclear translocator (ARNT). The AHR-ARNT heteroduplex is an environmental sensor that integrates extracellular, endogenous, and metabolic signals to equilibrate cell activity. Inactivation of AhR or ARNT increased TC cells' resistance to targeted therapies. Our study revealed that AhR-deficient cancer cells expressed elevated activity in genes linked to the TGFβ-mediated SMAD2/3 pathway after drug treatment. Our results suggest that SMAD2/3 competes to bind ARNT and that the loss of AhR gives cancer cells a potent escape pathway to targeted therapies, counteracting MAPK inhibition with SMAD activation to sustain cancer cell proliferation.

2025-01-12 | GSE286107 | GEO

Loss of the Aryl Hydrocarbon Receptor (AhR) Promotes Cancer Cells Resistance to BRAFV600E Targeted Therapies. [RNA-Seq]

2025-01-12 | GSE286108 | GEO

Loss of the Aryl Hydrocarbon Receptor (AhR) Promotes Cancer Cells Resistance to BRAFV600E Targeted Therapies. [CRISPR]

Project description:Loss of the Aryl Hydrocarbon Receptor (AhR) Promotes Cancer Cells Resistance to BRAFV600E Targeted Therapies. [CRISPR]

| PRJNA1207941 | ENA

Effect of aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of murine hematopoietic stem cells

Project description:As part of a study of the role of the aryl hydrocarbon receptor (Ahr) in maintenance and senescence of hematopoietic stem cells (HSC), global gene expression profiling was done with HSC isolated from Ahr-knockout and wild-type mice. HSC from young-adult (8 wk old) AhR-KO mice had changes in expression of many genes related to HSC maintenance, consistent with the phenotype observed in aging Ahr-KO mice: decreased survival rate, splenomegaly, increased circulating white blood cells, hematopoietic cell accumulation in tissues, anemia, increased numbers of stem/progenitor and lineage-committed cells in bone marrow, decreased erythroid progenitor cells in bone marrow, and decreased self-renewal capacity of HSC. 7 samples: 3 Ahr knockout, 4 wild-type

2013-11-08 | E-GEOD-46976 | biostudies-arrayexpress

Characterization of the aryl hydrocarbon receptor as a potential candidate to improve cancer T cell therapies

Project description:T cell-based cancer therapies efficacy can be limited by the tumor microenvironment which can lead to T cell dysfunction. Multiple studies, particularly in murine models, have demonstrated the capacity of the aryl hydrocarbon receptor (AhR) to negatively regulate antitumor T cell functions. AhR is a cytoplasmic receptor and transcription factor that was originally identified as a xenobiotic sensor, but has since been shown to play a significant role in the gene regulation of various immune cells, including T cells. Given the insights from murine studies, AhR emerges as a promising candidate to invalidate for optimizing T cell-based cancer therapies. However, the lack of studies on the role of AhR in human T cells underscores the need for comprehensive characterization of AhR expressing T cells. This study aims to investigate the regulatory mechanisms of AhR in human T cell biology to better understand its impact on reducing antitumor immune responses. By using the CRISPR-Cas method, knockout was performed on human T cells in order to characterize Ahr knocked-out T cells using an in vitro chronic stimulation model. Engineered T cells exhibited enhanced effector- and memory-like profiles and expressed reduced amount of CD39 and TIGIT. Ahr knockout enhanced human CAR-T cells’ functionality and persistence upon tumor chronic stimulation. Collectively, these results highlight the role of AhR in human CAR-T cells efficiency.

2025-05-16 | GSE279526 | GEO

Effect of aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of aged (18-month-old) murine hematopoietic stem cells

Project description:As part of a study of the role of the aryl hydrocarbon receptor (Ahr) in maintenance and senescence of hematopoietic stem cells (HSC), global gene expression profiling was done with HSC isolated from 18-month-old Ahr-knockout and wild-type mice. HSC from aged AhR-KO mice had changes in expression of many genes related to HSC maintenance, consistent with the phenotype observed in aging Ahr-KO mice: decreased survival rate, splenomegaly, increased circulating white blood cells, hematopoietic cell accumulation in tissues, anemia, increased numbers of stem/progenitor and lineage-committed cells in bone marrow, decreased erythroid progenitor cells in bone marrow, and decreased self-renewal capacity of HSC. 10 samples: 5 Ahr knockout, 5 wild-type

2015-03-28 | E-GEOD-67378 | biostudies-arrayexpress

RNAseq analysis of human CD14+ monocytes exposed to an agonist of Aryl Hydrocarbon Receptor

Project description:Aryl Hydrocarbon Receptor (AhR) is a ligand-activated transcription factor. To understand what genes are controlled by AhR in human monocytes, we performed transcriptomic analysis.

2025-08-12 | GSE214091 | GEO

Effect of aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of murine hematopoietic stem cells

2013-11-08 | GSE46976 | GEO

Aryl hydrocarbon receptor (AHR)-dependent protection against lung vascular leakage in viral infection

Project description:Disruption of the lung endothelial-epithelial cell barrier during respiratory virus infection causes cell and fluid accumulation in the air spaces and compromises vital gas exchange function. Endothelial cell dysfunction is known to exacerbate tissue damage; however, it is unclear whether the lung endothelium engages in tissue-protective activity during viral infection. Here we show that the environmental sensor aryl hydrocarbon receptor (AHR) is predominantly active in endothelial cells and protects against influenza-induced lung damage. Endothelial-specific AHR deletion caused increased vascular leakage in air spaces and enhanced influenza-induced lung tissue pathology. Global expression profiling revealed limited AHR-dependent regulation of vessels in the steady-state lung. However, following influenza-induced tissue damage and inflammation, AHR engages tissue-protective programmes in endothelia and prevents a dysplastic keratinised and apoptotic signature in the airways of infected lungs.

2023-05-23 | GSE203427 | GEO

Effect of bone marrow-specific aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of hematopoietic stem cells from young and old mice.

Project description:As part of a study of the role of the aryl hydrocarbon receptor (Ahr) in maintenance and senescence of hematopoietic stem cells (HSC), global gene expression profiling was done with HSC isolated from bone marrow restricted conditional Ahr-knockout and AhR floxed mice. HSC from young-adult (8 wk old) cAhR-KO mice had changes in expression of many genes related to HSC maintenance, consistent with the phenotype observed in Ahr-KO mice. Aged cAhR-KO mice (18 months old) also displayed alterations in peripheral white blood cell counts, serial repopulation potential and levels of ROS in bone marrow cells, consistent with previous observations on the role of AhR in the hematopoietic system. 22 samples: 5 young Ahr knockout, 6 old Ahr knockout, 5 young floxed Ahr, 6 old floxed Ahr

2016-06-30 | E-GEOD-76276 | biostudies-arrayexpress

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