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DAB2IP Loss in Luminal A Breast Cancer Leads to NF-kB- Associated Aggressive Oncogenic Phenotypes

ABSTRACT: DAB2IP Loss in Luminal A Breast Cancer Leads to NF-kB- Associated Aggressive Oncogenic Phenotypes

PROVIDER: PRJNA947218 | ENA |

REPOSITORIES: ENA

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DAB2IP Loss in Luminal A Breast Cancer Leads to NF-kB- Associated Aggressive Oncogenic Phenotypes

Project description:Despite proven therapy options for estrogen receptor (ER)-positive tumors, a significant number of patients with these cancers exhibit relapse with associated metastasis. Studies have shown that the loss of expression of RasGAPs leads to aggressive phenotypes and poor outcomes in several cancers including breast cancer. In our study, mining TCGA gene expression profiles of ER-positive breast tumors, we found that low expression of the RasGAP, DAB2IP is associated with a significant decrease in relapse-free survival in patients with Luminal A breast tumors. Immunostaining found that DAB2IP loss occurs in grade 2 tumors and higher. Consistent with this, genes upregulated in low DAB2IP Luminal A tumors are shared with more aggressive tumor subtypes, and are associated with proliferation, metastasis, and enhanced ER-signaling. In addition, cell-based studies reveal that low DAB2IP expression in ER-positive breast cancer cells is associated with increased proliferation, enhanced stemness phenotypes, and activation of IKK, the upstream regulator of the NF-B signaling pathway. Further, integrating cell-based ChIP-seq with motif analysis and TCGA RNA-seq data, we identify a candidate set of NF-B target genes that are upregulated with loss of DAB2IP and are proposed to regulate several oncogenic phenotypes, including altered RNA processing. This study provides new insight into mechanisms associated with aggressiveness and recurrence within a subset of Luminal A breast cancers that are otherwise typically less aggressive. Gene expression profiling by RNA-sequencing of DAB2IP knockdown and control MCF10A cells.

2024-12-18 | GSE227876 | GEO

DAB2IP Loss in Luminal A Breast Cancer Leads to NF-kB- Associated Aggressive Oncogenic Phenotypes

2024-12-18 | GSE227875 | GEO

DAB2IP Loss in Luminal A Breast Cancer Leads to NF-kB- Associated Aggressive Oncogenic Phenotypes

Project description:DAB2IP Loss in Luminal A Breast Cancer Leads to NF-kB- Associated Aggressive Oncogenic Phenotypes

| PRJNA947220 | ENA

DAB2IP Loss in Luminal A Breast Cancer Leads to NF-kB- Associated Aggressive Oncogenic Phenotypes

Project description:DAB2IP Loss in Luminal A Breast Cancer Leads to NF-kB- Associated Aggressive Oncogenic Phenotypes

| PRJNA947221 | ENA

DAB2IP Loss in Luminal A Breast Cancer Leads to NF-kB- Associated Aggressive Oncogenic Phenotypes

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-12-18 | GSE227877 | GEO

Effects of DAB2IP expression on gene expression in DLD1 cells

Project description:To assess the function of DAB2IP in colon cancer, we expressed DAB2IP or control LACZ in DLD1 cells which lack DAB2IP.

2023-03-05 | GSE224869 | GEO

Effects of DAB2IP depletion on gene expression in HCT116 cells

Project description:To study DAB2IP function on colon cancer, we depleted DAB2IP in HCT116 cells using shDAB2IP or shCNT(scramble) as a control.

2023-03-05 | GSE224870 | GEO

Benchmarking NF-kB inhibitors

Project description:Benchmarking NF-kB inhibitors

| PRJNA562687 | ENA

GSF1635: RNA-seq data of OVCAR3-DAB2IP expressing cells vs. control

Project description:Ovarian cancer (OC) is the leading cause of death from gynecologic malignancies in the US. Ovarian cancer stem cells (OCSCs) have been shown to drive chemoresistance and tumor progression but the mechanism remains incompletely understood. Disabled Homolog 2- Interacting Protein (DAB2IP) is a potent tumor suppressor identified in multiple types of cancers and we demonstrate that DAB2IP is silenced by the repressive epigenetic mark H3K27me3 at the DAB2IP promoter loci in OCSCs.

2020-09-30 | GSE144948 | GEO

A Basal Stem Cell Signature Identifies Aggressive Prostate Cancer Phenotypes

Project description:Aggressive cancers and normal stem cells often share similar molecular and functional traits. It is unclear if aggressive phenotypes of prostate cancer molecularly resemble normal stem cells residing within the human prostate. We performed high-throughput RNA sequencing on uncultured, highly purified epithelial populations from human prostates obtained after radical prostatectomy. We found the basal population to be defined by genes associated with developmental programs, epigenetic remodeling, and invasiveness. We further generated a 91-gene basal signature and applied it to gene expression datasets from patients with organ-confined or castration-resistant, metastatic prostate cancer. Metastatic prostate cancer was more enriched for the basal stem cell signature than organ-confined prostate cancer. Moreover, histological subtypes within prostate cancer metastases varied in their enrichment of the stem cell signature with small cell neuroendocrine carcinoma being the most stem cell-like. Bioinformatic analysis of the basal cell and two human small cell gene signatures identified a set of E2F target genes common to all three signatures. These results suggest that the most aggressive variants of prostate cancer share a core transcriptional program with normal prostate basal stem cells. Transcriptional analysis of 10 uncultured prostatic basal and luminal populations from either the benign or malignant prostate tissue of 8 human prostate cancer patients by high-throughput RNA-seq

2016-06-01 | E-GEOD-82071 | biostudies-arrayexpress

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