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

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

PROVIDER: PRJNA1160264 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30650605_1.fastq.gz	Fastqsanger.gz
	SRR30650605_2.fastq.gz	Fastqsanger.gz
	SRR30650606_1.fastq.gz	Fastqsanger.gz
	SRR30650606_2.fastq.gz	Fastqsanger.gz
	SRR30650607_1.fastq.gz	Fastqsanger.gz

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

Project description: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.

2025-01-15 | GSE277029 | GEO

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 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

TonEBP increases TRIM37

Project description:TonEBP increases TRIM37

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

2014-10-06 | GSE48196 | GEO

Mesoscale regulation of microtubule-organising centres by the E3 ligase TRIM37

Project description:Centrosomes ensure accurate chromosome segregation during cell division. Although the regulation of centrosome number is well-established, less is known about the suppression of non-centrosomal Microtubule-Organising Centres (ncMTOCs). The E3 ligase TRIM37, implicated in Mulibrey nanism and 17q23-amplified cancers, has emerged as a key regulator of both centrosomes and ncMTOCs. Yet, the mechanism by which TRIM37 achieves enzymatic activation to target these mesoscale structures had thus far remained unknown. Here, we elucidate the activation process of TRIM37, unveiling a process that initiates with TRAF domain-directed substrate recognition, followed by B-box domain-mediated oligomerisation, and culminates in RING domain dimerisation. Using optogenetics, we demonstrate that the E3 activity of TRIM37 is directly coupled to the assembly state of its substrates, being activated only when centrosomal proteins cluster into higher-order assemblies resembling MTOCs. This regulatory framework provides a mechanistic basis for understanding TRIM37-driven pathologies and echoes the restriction of the HIV capsid by TRIM5, thus unveiling a conserved activation blueprint among TRIM proteins to control turnover of complexes assembled at the mesoscale level.

2025-03-18 | PXD061083 | Pride

TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression [RNA-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 | GSE182545 | GEO

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

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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

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

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