Role of Id1 and Id3 in breast cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA533060 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8906390_1.fastq.gz | Fastqsanger.gz | |||
| SRR8906390_2.fastq.gz | Fastqsanger.gz | |||
| SRR8906400_1.fastq.gz | Fastqsanger.gz | |||
| SRR8906400_2.fastq.gz | Fastqsanger.gz | |||
| SRR8906391_1.fastq.gz | Fastqsanger.gz |
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Project description:By combining RNAi-mediated knockdown of Id1 and Id3 in an aggressive mouse breast cancer cell line (4T1 cells) with genome-wide expression profiling, we identified several new Id target genes and novel pathways regulated by Id.
2020-10-31 | GSE129790 | GEO
Project description:Cyclin D1 is a well characterised cell cycle regulator with established oncogenic capabilities. Despite these properties, studies report contrasting links to tumour aggressiveness. It has previously been shown that silencing cyclin D1 increases the migratory capacity of MDA-MB-231 breast cancer cells with concomitant increase in ‘inhibitor of differentiation 1’ (ID1) gene expression. Id1 is known to be associated with more invasive features of cancer and with the epithelial-mesenchymal transition (EMT). Here, we sought to determine if the increase in cell motility following cyclin D1 silencing was mediated by Id1 and enhanced EMT-features. To further substantiate these findings we aimed to delineate the link between CCND1, ID1 and EMT, as well as clinical properties in primary breast cancer. The increase in cell migration following cyclin D1 silencing in MDA-MB-231 cells was abolished by Id1 siRNA treatment and we observed cyclin D1 occupancy of the Id1 promoter region. Moreover, ID1 and SNAI2 gene expression was increased following cyclin D1 knock-down, an effect reversed with Id1 siRNA treatment. Similar migratory and SNAI2 increases were noted for the ER-positive ZR75-1 cell line, but in an Id1 independent manner. In a meta-analysis of 1107 breast cancer samples, CCND1 and ID1 gene expression were associated with mesenchymal-markers including SNAI1, SNAI2 and TWIST1, and with clinicopathological parameters. Finally, a greater percentage of CCND1low/ID1high tumours were found in the EMT-like ‘claudin-low’ subtype of breast cancer than in other subtypes. Together, these results indicate that increased migration of MDA-MB-231 cells following cyclin D1 silencing can be mediated by Id1 and is linked to an increase in EMT markers. Moreover, we have confirmed a relationship between cyclin D1, Id1 and EMT in primary breast cancer, supporting our in vitro findings that low cyclin D1 expression can be linked to aggressive features in subgroups of breast cancer. MDA-MB-231 cells were transfected with cyclin D1, CDK4/6 or control siRNA.
2011-10-12 | E-GEOD-27260 | biostudies-arrayexpress
Project description:Cyclin D1 is a well characterised cell cycle regulator with established oncogenic capabilities. Despite these properties, studies report contrasting links to tumour aggressiveness. It has previously been shown that silencing cyclin D1 increases the migratory capacity of MDA-MB-231 breast cancer cells with concomitant increase in ‘inhibitor of differentiation 1’ (ID1) gene expression. Id1 is known to be associated with more invasive features of cancer and with the epithelial-mesenchymal transition (EMT). Here, we sought to determine if the increase in cell motility following cyclin D1 silencing was mediated by Id1 and enhanced EMT-features. To further substantiate these findings we aimed to delineate the link between CCND1, ID1 and EMT, as well as clinical properties in primary breast cancer. The increase in cell migration following cyclin D1 silencing in MDA-MB-231 cells was abolished by Id1 siRNA treatment and we observed cyclin D1 occupancy of the Id1 promoter region. Moreover, ID1 and SNAI2 gene expression was increased following cyclin D1 knock-down, an effect reversed with Id1 siRNA treatment. Similar migratory and SNAI2 increases were noted for the ER-positive ZR75-1 cell line, but in an Id1 independent manner. In a meta-analysis of 1107 breast cancer samples, CCND1 and ID1 gene expression were associated with mesenchymal-markers including SNAI1, SNAI2 and TWIST1, and with clinicopathological parameters. Finally, a greater percentage of CCND1low/ID1high tumours were found in the EMT-like ‘claudin-low’ subtype of breast cancer than in other subtypes. Together, these results indicate that increased migration of MDA-MB-231 cells following cyclin D1 silencing can be mediated by Id1 and is linked to an increase in EMT markers. Moreover, we have confirmed a relationship between cyclin D1, Id1 and EMT in primary breast cancer, supporting our in vitro findings that low cyclin D1 expression can be linked to aggressive features in subgroups of breast cancer.
2011-10-13 | GSE27260 | GEO
Project description:The diagnosis of B-Cell acute lymphoblastic leukemia (B-ALL) in adults often carries a poor prognosis. ID1 and ID3 genes have been identified as predictors of poor response in Colombian adult B-ALL patients, playing roles in cancer development. In different cancer models, these genes have been associated with immune regulator populations within the tumor immune microenvironment (TIME). B-ALL development alters the immune cell composition and the bone marrow (BM) tumor microenvironment, affecting disease progression and response to therapy. This study analyzes gene expression levels of ID1 and ID3 in relation to TIME and immune evasion. This exploratory study analyzed BM samples from 10 B-ALL adult patients diagnosed at the National Cancer Institute of Colombia. First, RT-qPCR was used to assess ID1 and ID3 expression in BM tumor cells. Flow cytometry characterized immune populations in the TIME. RNA-seq evaluated immune genes associated with B-ALL immune response, while xCell and cytosig analyzed TIME cell profiles and cytokines. Pathway analysis, gene ontology, and differential gene expression (DEGs) were examined, with functional enrichment analysis performed using KEGG ontology. Patients were divided into two groups based on ID1 and ID3 expression, namely basal and overexpression. A total of 94 differentially expressed genes were identified between these groups, with top overexpressed genes associated with neutrophil pathways. Gene set enrichment analysis revealed increased expression of genes associated with neutrophil degranulation, immune response-related neutrophil activation, and neutrophil-mediated immunity. These findings correlated with xCell data. Overexpression group showed significant differences in neutrophils (p=0.0008), monocytes (<0.0001) and CD4+ naive T cells (p=0.0240) compared to basal group patients. Microenvironment and immune scores were also significantly different (p=0.0016 and p=0.0017, respectively), consistent with the flow cytometry results. Elevated cytokine levels associated with neutrophil activation supported these findings. Validation was performed using the TARGET and MILE B-ALL cohorts. Our results show important differences between the expression level of ID1 and ID3 in cancer cells and the populations of TIME, suggesting a role in evading the immune response of ID1 and ID3 in B-ALL, mainly related to neutrophil pathways.
2024-11-08 | GSE276392 | GEO
Project description:Single cell RNA-Seq was performed on ID1 ID3 null endothelial cells to determine the effects of ID gene loss on endothelial cell maintainence and growth.
2020-04-22 | GSE149030 | GEO
Project description:Rationale: The Id1 and Id3 genes play major roles during cardiac development, despite their expression being confined to non-myocardial layers (endocardium – endothelium - epicardium). We previously described that Id1–/–Id3–/– double knockout (dKO) mouse embryos die at mid-gestation from multiple cardiac defects, but early demise precluded the studies of the roles of Id in the adult mice. Objective: To elucidate postnatal roles of Id genes in the heart. Methods and Results: We ablated Id1 gene in the vasculature and Id3 gene globally to generate Tie2Cre+Id1F/–Id3–/– and Tie2Cre+Id1F/FId3–/– conditional KO (Id cKO) embryos. Half of the Id cKO mice die at birth. Postnatal demise was associated with cardiac underdevelopment, enlargement, muscular ventricular septal and endothelial defects. Surviving Id cKO mice exhibited dilated, fibrotic cardiomyopathy associated with defects in the vasculature. The adult cardiac phenotype progressed into heart failure and resembled endomyocardial fibroelastosis. An abnormal vascular response was also observed in the healing process of excisional skin wounds of Id cKO mice. Expression patterns of vascular, fibrotic and hypertrophic markers were altered in the Id cKO hearts, but addition of Insulin-Like Growth Factor binding protein-3 (IGFbp3) reversed gene expression profiles of vascular and fibrotic, but not hypertrophic markers. Conclusions: Conditional ablation of Id genes in the vasculature leads to dilated fibrotic cardiomyopathy. The findings could reveal important insights into the role(s) of the endocardial network of the endothelial lineage to the development of dilated fibrotic cardiomyopathy and identify a potential therapeutic target, IGFbp3, in its treatment.
2010-10-07 | GSE21924 | GEO
Project description:Id1 and its closely related family member Id3 are expressed by a diversity of stem and progenitor cells. We show that Id1/3 are required for the self-renewal and proliferation of triple negative breast cancer (TNBC) cells both in vitro and in vivo. Furthermore, we identified that Id1/3 negatively regulates the tumour suppressor gene Robo1. Depletion of Robo1 could rescue the proliferative defect induced by Id1/3 knockdown. To understand the mechanisms by which Robo1 rescues cell proliferation in Id1/3 depleted cells, we performed RNA-Sequencing on 4T1 cells with Dox-inducible Id1/3 KD and/or Robo1 depletion using siRNA. We conclude that following Id1/3 knockdown, Robo1 is induced and exerts anti-proliferative effects via suppression of a Myc transcriptional program.
2020-10-31 | GSE129858 | GEO
Project description:TCF3 belongs to E protein family and has the function of transcription factor. TCF3 can directly interact with HLH family proteins ID1 and ID3 to play biological functions. ID1 and ID3 do not have the ability to directly bind to DNA and need to be regulated by TCF3. We found changes in pluripotency in ID1 and ID3 double knockout lines of human ESC, so we suspected that ID1 / 3 played a regulatory role through TCF3. Therefore, TCF3 ChIP-seq was done in WT and KO lines, hoping to find the downstream genes regulated by ID1 / 3 through TCF3, and then regulate hESC pluripotency through these genes.
2022-06-27 | GSE183518 | GEO
Project description:To gain insights into the genetic program activated within the distinct vascular and inflammatory transplant microenvironments in Id1/Id3 deficient and WT mice, we performed a series of gene screening experiments using RNA from total graft tissue as well as from myeloid and endothelial (i.e., CD31+ and ISB4+) cells isolated from the grafts at 1 week post-transplantation.
2008-06-13 | E-TABM-355 | biostudies-arrayexpress
Project description:Genome-wide expression profiling of 4T1 cells to identify genes that are regulated by Id1 and Id3 in breast cancer
| PRJNA532835 | ENA