Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-MTAB-11344

ABSTRACT: ROBO3s: a novel ROBO3 shot isoform promoting breast cancer aggressiveness

PROVIDER: E-MTAB-11344 | ExpressionAtlas | 2025-06-09

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-MTAB-11344-analysis-methods.tsv	Tabular
	E-MTAB-11344-analytics.tsv	Tabular
	E-MTAB-11344-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-11344-configuration.xml	Xml
	E-MTAB-11344-g2_g1-mvaPlot.png	Other

Items per page:

1 - 5 of 22

Similar Datasets

ROBO3s: a novel ROBO3 shot isoform promoting breast cancer aggressiveness

Project description:ROBO3s: a novel ROBO3 shot isoform promoting breast cancer aggressiveness

| PRJEB46393 | ENA

ROBO3s: a novel ROBO3 shot isoform promoting breast cancer aggressiveness

Project description:ROBO3s: a novel ROBO3 shot isoform promoting breast cancer aggressiveness

| PRJEB50323 | ENA

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)

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 | 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 (ncRNA-Seq)

2021-08-19 | GSE178250 | GEO

Homo sapiens

Project description:Breast cancer tumor promoting cell transcriptome

| PRJNA252386 | ENA

TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression [ChIP-seq]

Project description:Using a proteomics approach, we identified the Tripartite Motif Containing 37 (TRIM37) as a novel transcriptional coactivator of AP-2γ. We demonstrate TRIM37 facilitates AP-2γ chromatin binding to regulate the AP-2γ mediated transcriptional program directly. We provide evidence that TRIM37 achieves this by stimulating K63-chain-linked polyubiquitination of AP-2γ, promoting protein localization from the cytoplasm to the nucleus. In clinical analyses, we find TRIM37 is upregulated in multiple breast cancer datasets, supporting our findings that TRIM37-AP-2γ interaction is essential for breast cancer tumor growth. Overall, our work revealed that TRIM37 is an oncogenic coactivator of AP-2γ in breast cancer and provides a novel therapeutic target for treating the disease.

2022-07-25 | GSE182546 | GEO

Effect of DC-SCRIPT expression in MCF7 breast cancer cell line

Project description:Breast cancer is one of the most common causes of cancer-related deaths in women. Nuclear receptors (NR) and their regulators are well known for their role in breast cancer. Especially ligands for the type I NRs, Estrogen Receptor (ER) and Progesterone Receptor have growth promoting effects in breast cancer cells. The NR coregulator DC-SCRIPT (ZNF366) has been found to be a strong and independent prognostic marker in ER positive (ESR1) breast cancer patients. DC-SCRIPT modulates the function of multiple NRs and has opposing effects on type I versus type II NRs. It represses the function of the growth promoting type I NRs, whereas it enhances the mainly anti-proliferative type II NRs. In this study we aimed to gain further insight into the functional role of DC-SCRIPT in breast cancer cells. Therefore, the effect of DC-SCRIPT expression on breast cancer cell gene expression was investigated using a novel DC-SCRIPT-inducible MCF7 breast cancer cell line model. In the presence of DC-SCRIPT, multiple cell cycle related genes were differentially expressed, including the tumor suppressor gene CDKN2B. MCF7EV (empty vector control) and MCF7SC (DC-SCRIPT-inducible) breast cancer cell lines were treated with doxycyline for a total of 68h (to induce DC-SCRIPT expression in MCF7SC clones). After the first 24h, cells were serum starved for 24h to synchronize the cells. Subsequently, cells were released with 10 nM estradiol during the last 20 hours of culturing. Total RNA from two replicate experiments were obtained, and used to compare MCF7EV to MCF7SC clones.

2015-08-01 | E-GEOD-59995 | biostudies-arrayexpress

Tumor-associated neutrophil precursors impair homologous DNA repair and promote sensitivity to PARP-inhibition [ChIP-seq]

Project description:Tumor evolution is one of the major mechanisms responsible for acquiring therapy-resistant and more aggressive cancer clones. Whether the tumor microenvironment through immune-mediated mechanisms might promote the development of more aggressive cancer types is crucial for the identification of additional therapeutical opportunities. Here, we identified a novel subset of tumor-associated neutrophils, defined as tumor-associated neutrophil precursors (PreNeu). These PreNeu are enriched in female highly proliferative hormone-dependent breast cancers and impair DNA repair capacity.  Mechanistically, succinate secreted by tumor-associated PreNeu inhibit homologous recombination, promoting error-prone DNA repair through non-homologous end-joining regulated by PARP-1. Consequently, breast cancer cells acquire genomic instability promoting tumor editing and progression. Selective inhibition of these pathways induces increased tumor cell killing in vitro and in vivo. Tumor-associated PreNeu score correlates with copy number alterations in highly proliferative hormone-dependent tumors from breast cancer patients. Treatment with PARP-1 inhibitors counteract the pro-tumoral effect of these neutrophils.

2025-03-18 | GSE288568 | GEO

Effect of DC-SCRIPT expression in MCF7 breast cancer cell line

2015-08-01 | GSE59995 | 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