Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A TRIM37 risk variant rs57141087 contributes to triple-negative breast cancer onset and progression in Black women.

ABSTRACT: TRIM37 is a histone H2A ubiquitin ligase importantin breast cancer oncogenesis. To assess the neoplastic transformationsof normal breast epithelial cells in the context of TRIM37, we increased its expression and compared the gene expression network regulated by TRIM37 in control and TRIM37 overexpression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE277029 | GEO | 2025/01/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

TRIM37 is a novel H2A ubiquitin ligase and a Breast Cancer Oncogene

Project description:The TRIM37 gene is mutatedin Mulbery nanism, a rare autosomal recessive disorder, and is in the 17q23 chromosomal region that is amplified in up to ~40% of breast cancers. Trim37 contains a RING finger domain, a hallmark of E3 ubiquitin ligases, but the protein substrate(s) of Trim37 is unknown. Mono-ubiquitination of histone H2A is a chromatin modification associated with transcriptional repression and here we report that Trim37 is an H2A ubiquitin ligase. Genome-wide Chip-CHIP experiments indicate that in human breast cancer cells containing amplified 17q23, Trim37 is bound to the promoters of many tumor suppressor genes. RNA interference (RNAi)-mediated knockdown of Trim37 results in loss of ubiquitinated H2A, dissociation of PRC1 and PRC2, and transcriptional reactivation of silenced genes. Knockdown of Trim37 in human breast cancer cells containing amplified 17q23 substantially decreases tumor growth in mouse xenografts. Collectively, our results reveal Trim37 as a new H2A ubiquitin ligase that is overexpressed in a subset of breast cancers and redirects PRC2 to silence tumor suppressors and other genes resulting in oncogenesis. Identification of TRIM37 Binding targets in MCF7 cells from the two replicate experiments

2014-10-06 | E-GEOD-48196 | biostudies-arrayexpress

TRIM37 is a novel H2A ubiquitin ligase and a Breast Cancer Oncogene

2014-10-06 | GSE48196 | GEO

RNA-seq analysis of MDA-MB-231_2b cells treated with control or TRIM37 specific antisense oligonucleotides

Project description:TRIM37 is histon H2A ubiquitinase and important oncogene for breast cancer. To test what is the gene expression network regulated by TRIM37, we silenced its ixpression in MDA-MB-231_2b Triple Negative Breast Cancer (TNBC) cell line.

2022-08-31 | GSE136617 | GEO

A TRIM37 risk variant rs57141087 contributes to triple-negative breast cancer onset and progression in Black women.

Project description:A TRIM37 risk variant rs57141087 contributes to triple-negative breast cancer onset and progression in Black women.

| PRJNA1160264 | ENA

The TRIM37 variant rs57141087 contributes to triple-negative breast cancer outcomes in Black women

Project description:Triple-negative breast cancer (TNBC) disproportionately affects younger Black women, who show more aggressive phenotypes and poorer outcomes than women of other racial identities. While the impact of socioenvironmental inequities within and beyond health systems is well documented, the genetic influence in TNBC-associated racial disparities remains elusive. Here, we report that cancer-free breast tissue from Black women expresses TRIM37 at a significantly higher level relative to White women. A reporter-based screen for regulatory variants identifies a non-coding risk variant rs57141087 in the 5' gene upstream region of the TRIM37 locus with enhancer activity. Mechanistically, rs57141087 increases enhancer-promoter interactions through NRF1, resulting in stronger TRIM37 promoter activity. Phenotypically, high TRIM37 levels drive neoplastic transformations in immortalized breast epithelial cells. Finally, context-dependent TRIM37 expression reveals that early-stage TRIM37 levels affect the initiation and trajectory of breast cancer progression. Together, our results indicate a genotype-informed association of oncogenic TRIM37 with TNBC risk in Black women and implicate TRIM37 as a predictive biomarker to better identify patients at risk of aggressive TNBC.

| S-SCDT-10_1038-S44319-024-00331-2 | biostudies-other

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

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

2022-07-25 | GSE182545 | GEO

TonEBP increases TRIM37

Project description:TonEBP increases TRIM37

| PRJNA896497 | ENA

LSD1 maintains mammary luminal cell differentiation and suppresses luminal breast cancer cell invasion

Project description:LSD1 (KDM1A) is a histone demethylase that plays both oncogenic and tumor suppressor roles in breast cancer. However, the exact contexts under which it plays these opposite roles remain largely elusive. By characterizing its role in normal and cancerous luminal mammary epithelial cells (MECs), here we show that LSD1 is essential for maintaining differentiation and survival of luminal cells. LSD1-inhibition by both genetic and pharmacological approaches increases invasion of luminal breast cancer cells. Mechanistically, we find LSD1 interacts with GATA3 and their common target genes are highly related to breast cancer. LSD1 positively regulates GATA3 expression and represses that of TRIM37, a histone H2A ubiquitin ligase and breast cancer oncoprotein. LSD1-loss leads to reduced expression of several cell junction genes (e.g., CDH1, VCL, CTNNA1), possibly via TRIM37-mediated repression. Collectively, our data suggest LSD1 largely plays a tumor suppressor role in luminal breast cancer and the increased MEC invasiveness associated with LSD1-inhibition can be blocked via TRIM37-inhibition.

2019-08-16 | GSE95165 | GEO

The ubiquitin ligase TRIM37 controls cancer-specific vulnerability to PLK4 inhibition

Project description:We show synthetic lethality between PLK4 inhibition-mediated centrosome loss and the overexpression of the ubiquitin ligase TRIM37 in cancer cells with amplification of Chr17q

2020-09-18 | GSE148263 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data