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Dichotomous roles of Arid5a augment the immunosuppressive microenvironment of mesenchymal malignant tumors

ABSTRACT: Dichotomous roles of Arid5a augment the immunosuppressive microenvironment of mesenchymal malignant tumors

PROVIDER: PRJNA670964 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12885017.fastq.gz	Fastqsanger.gz
	SRR12885018.fastq.gz	Fastqsanger.gz
	SRR12885019.fastq.gz	Fastqsanger.gz
	SRR12885020.fastq.gz	Fastqsanger.gz
	SRR12885021.fastq.gz	Fastqsanger.gz

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Dichotomous roles of Arid5a augment the immunosuppressive microenvironment of mesenchymal malignant tumors

Project description:Although mesenchymal subtypes of pancreatic ductal adenocarcinoma (PDAC) and colorectal cancer (CRC) are known as “immunologically cold” tumors, the molecular link between tumor immune evasiveness and mesenchymal phenotype remains largely unknown. Here, we show that AT-rich interaction domain-containing protein 5a (Arid5a), an RNA-binding protein, is involved in immune evasion in PDAC and CRC mouse models. Mass cytometry demonstrated that in tumors from Arid5a-deficient cells, the infiltration of granulocytic myeloid-derived suppressor cells and regulatory T cells is suppressed, but cytotoxic T-lymphocyte recruitment is enhanced. Mechanistically, Arid5a augmented Ido1 and Ccl2 expression by stabilizing these mRNAs in the PDAC model, but not Ido1 in the CRC model. Furthermore, Arid5a expression was substantially increased in mesenchymal subtypes of PDAC and CRC, mediated by ZEB1, and Arid5a promoted TGF-b-induced and IL6-induced epithelial-mesenchymal transition and acquisition of invasiveness in PDAC model cells. Thus, our findings demonstrate that Arid5a is a promising target for immunotolerant malignant tumors.

2021-04-07 | GSE159967 | GEO

Arid5a directs autoimmune inflammation through an IL-17 signaling pathway [mouse]

Project description:Using Arid5a deficient mice to study the role of the RNA-binding protein Arid5a in models of autoimmunity, namely autoimmune glomerulonephritis

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Arid5a directs autoimmune inflammation through an IL-17 signaling pathway [human]

Project description:Using Arid5a deficient mice to study the role of the RNA-binding protein Arid5a in models of autoimmunity, namely autoimmune glomerulonephritis

2024-07-15 | GSE269728 | GEO

Transcriptome-wide mapping of RNA:protein interactions of Arid5a in mouse P19 cells.

Project description:We performed Arid5a iCLIP2 in P19 cells transiently expressing GFP-tagged Arid5a.

2024-08-01 | GSE254818 | GEO

The disordered extensions of the Arid5a core ARID domain modulate its DNA- and RNA-binding propensities

Project description:ARID (AT-rich interacting domain) proteins are a heterogeneous family of DNA-binding proteins involved in transcriptional regulation. No precise DNA-binding preferences have yet been defined for the aberrant member Arid5a. In addition, the protein binds to mRNA motifs for transcript stabilisation, presumably through the DNA-binding ARID domain. Here we first provide an unbiased definition of RNA motifs and a clear breakdown of nucleic acid binding by the ARID domain. An RNA Bind-n-Seq (RBNS) experiment was performed to find a consensus motif of the Arid5a domain. It reveals a preference for an unexpected CAGGCAG consensus motif, accompanied by a general preference for AU-rich motifs.

2024-03-21 | GSE256029 | GEO

The novel long noncoding RNA lncRNA-AU021063, induced by IL-6/Arid5a signaling, exacerbates breast cancer invasion and metastasis by stabilizing Trib3 and activating the Mek/Erk pathway (ncRNA-Seq)

Project description:Interleukin (IL-6) is a pleotropic cytokine with both tumor-promoting and -inhibitory effects on breast cancer growth. However, the mechanisms governing the outcome of IL-6 on cancer progression remain to be clarified. Our study unraveled a novel long noncoding RNA (lncRNA)-AU021063 downstream of IL-6 signaling. We found that IL-6 induced the expression of lncRNA-AU021063 predominantly in breast cancer compared to other cancer types. Mechanistically, IL-6 induced AT-rich interactive domain 5a (Arid5a) expression, which promotes the transcription of lncRNA-AU021063. In turn, lncRNA-AU021063 promotes breast cancer metastasis through stabilizing tribbles homolog 3 (Trib3) and activating Mek/Erk signaling pathway. Genetic ablation of either Arid5a, lncRNA-AU021063 or Trib3 abolished breast cancer metastasis in vitro and in vivo. Overall, our study highlights the importance of IL-6-Arid5a-lncRNA-AU021063 axis in regulating breast cancer invasiveness and metastasis, which may provide potential novel therapeutics for breast cancer.

2021-08-19 | GSE178250 | GEO

The novel long noncoding RNA lncRNA-AU021063, induced by IL-6/Arid5a signaling, exacerbates breast cancer invasion and metastasis by stabilizing Trib3 and activating the Mek/Erk pathway (ChIP-Seq)

2021-08-19 | GSE178249 | GEO

The novel long noncoding RNA lncRNA-AU021063, induced by IL-6/Arid5a signaling, exacerbates breast cancer invasion and metastasis by stabilizing Trib3 and activating the Mek/Erk pathway (mRNA-Seq)

2021-08-19 | GSE178251 | GEO

Dichotomous Engagement of HDAC3 Activity Governs Inflammatory Responses

Project description:Dichotomous Engagement of HDAC3 Activity Governs Inflammatory Responses

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A dichotomous response to chronic fetal hypoxia preprograms aging already during kidney development

Project description:Hypoxia-induced intrauterine growth restriction increases the risk for chronic diseases in adults, affecting more than 140 million high altitude residents worldwide. Still, not much is known about the fetal mechanisms that prone these individuals to disease. Using bottom-up proteomics and the kidney as a readout, we delineated a dichotomous response to chronic hypoxic stress, comprising mechanisms that promote survival, but also induce premature senescence. Combined outcome is the manifestation of a predetermined aging phenotype already during fetal development. This aging phenotype is associated with a characteristic biomarker profile in tissue and blood serum samples, exploitable for targeting and monitoring disease.

2022-01-13 | PXD018999 | Pride

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