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ABSTRACT: Aryl hydrocarbon receptor suppresses lung cancer metastasis

PROVIDER: PRJNA576587 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10249835.fastq.gz	Fastqsanger.gz
	SRR10249836.fastq.gz	Fastqsanger.gz
	SRR10249837.fastq.gz	Fastqsanger.gz
	SRR10249838.fastq.gz	Fastqsanger.gz
	SRR10249839.fastq.gz	Fastqsanger.gz

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Aryl hydrocarbon receptor-interacting protein regulates tumorigenic and metastatic properties of colorectal cancer cells driving liver metastasis

Project description:Aryl hydrocarbon receptor-interacting protein (AIP), a putative positive intermediary in aryl hydrocarbon receptor-mediated signaling, is overexpressed in highly metastatic human KM12SM CRC cells, with high metastatic capacity to liver, and other highly metastatic CRC cells. Meta-analysis and immunohistochemistry were used to assess the relevance of this protein in CRC. Cellular functions and signaling mechanisms mediated by AIP were assessed by gain-of-function experiments and in vitro and in vivo experiments. A significant association of high AIP expression with poor CRC patients’ survival was observed. Gain-of-function and quantitative proteomics experiments demonstrated that AIP increased tumorigenic and metastatic properties of isogenic KM12C (poorly-metastatic) and KM12SM CRC cells. AIP overexpression dysregulated epithelial-to-mesenchymal (EMT) markers and induced several transcription factors and Cadherin-17 activation. The former induced the signaling activation of AKT, SRC, and JNK kinases to increase adhesion, migration and invasion of CRC cells. In vivo, AIP expressing KM12 cells induced tumor growth and liver metastasis. Furthermore, KM12C (poorly-metastatic) cells ectopically expressing AIP became metastatic to liver. Our data reveal new roles for AIP in regulating proteins associated with cancer and metastasis to induce tumorigenic and metastatic properties in colon cancer cells driving liver metastasis.

2023-05-10 | PXD031119 | Pride

AhR mediated changes in the murine lung dendritic cell transcriptome

Project description:Analysis of gene expression in isolated mouse lung dendritic cells isolated during influenza A virus infection, with and without activaiton of the aryl hydrocarbon receptor (AHR).

2018-12-18 | GSE123996 | GEO

Macrophages Promote Pre-Metastatic Niche Formation of Breast Cancer through AHR Activity

Project description:Macrophages that acquire an immunosuppressive phenotype are crucial for creating the pre-metastatic niche (PMN), which is essential for facilitating breast cancer metastasis to the distant organ. Our study showed that increased aryl hydrocarbon receptor (AHR) activity in lung macrophages is vital for establishing the immunosuppressive PMN in breast cancer. AHR activation led to higher PD-L1 expression on macrophages through directly binding to the promoter of Pdl1, subsequently, promoting Treg cell differentiation in the PMN. Mice with Ahr conditional deletion in macrophages had reduced lung metastasis of breast cancer. The elevated AHR level in PMN macrophages was induced by GM-CSF released from breast cancer cells, which activated STAT5 and prevented AHR ubiquitination in macrophages. In breast cancer patients, the expression of AHR and PD-L1 correlated with Treg cell infiltration, and high AHR expression was associated with a poor prognosis. Our findings uncover a previously unknown cellular and molecular mechanism through which macrophages establish the lung PMN in breast cancer.

2024-10-18 | GSE277589 | GEO

The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries

Project description:This SuperSeries is composed of the following subset Series: GSE15857: The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries: Kidney GSE15858: The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries: Liver Refer to individual Series

2010-05-05 | E-GEOD-15859 | biostudies-arrayexpress

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Aryl Hydrocarbon Receptor suppresses STING-mediated Type I IFN expression in Triple-Negative Breast Cancer

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Phosphorylation of AHR by PLK1 promotes metastasis of LUAD via DIO2-TH signaling

Project description:Metastasis of Lung adenocarcinoma (LUAD) is a major cause of death in patients. Aryl hydrocarbon receptor (AHR) is an important transcription factor involved in the initiation and progression of lung cancer. Polo-like kinase 1 (PLK1), a serine/threonine kinase, is an oncogene that promotes the malignancy of multiple cancer types. Nonetheless, the interaction between these two factors and significance in lung cancer remains to be determined. Here, we demonstrate that PLK1 phosphorylates AHR at S489 in LUAD, which leads to epithelial-mesenchymal transition (EMT) and metastatic events. RNA-seq analyses show that type 2 deiodinase (DIO2) is responsible for EMT and enhanced metastatic potential. DIO2 converts tetraiodothyronine (T4) to triiodothyronine (T3), which then activates thyroid hormone signaling. In vitro and in vivo experiments demonstrate that treatment with T3 or T4 promotes the metastasis of LUAD, whereas depletion of DIO2 or deiodinase inhibitor disrupts this property. Taken together, our results identify the phosphorylation of AHR by PLK1 as a mechanism leading to the progression of LUAD and provide possible therapeutic interventions for this event.

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Project description:Gene Expression Profiling of Interactions Between Estrogen- and Aryl hydrocarbon-Receptor Signalling Pathways

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AHR ChIP-Seq of female mouse liver following 2 hour TCDD exposure

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AHR ChIP-Seq of male mouse liver following 2 hour TCDD exposure

Project description:Aryl hydrocarbon receptor ChIP-Seq performed in livers of male mice gavaged with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 2hrs

2017-04-12 | GSE97634 | GEO

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