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TFE3 fusion proteins drive oxidative metabolism, ferroptosis resistance and general RNA synthesis in translocation renal cell carcinoma. [Cut and Tag/ChIP-seq]

ABSTRACT: TFE3 fusion proteins drive oxidative metabolism, ferroptosis resistance and general RNA synthesis in translocation renal cell carcinoma. [Cut and Tag/ChIP-seq]

PROVIDER: PRJNA1114638 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29124605_1.fastq.gz	Fastqsanger.gz
	SRR29124605_2.fastq.gz	Fastqsanger.gz
	SRR29124606_1.fastq.gz	Fastqsanger.gz
	SRR29124606_2.fastq.gz	Fastqsanger.gz
	SRR29124607_1.fastq.gz	Fastqsanger.gz

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TFE3 fusion proteins drive oxidative metabolism, ferroptosis resistance and general RNA synthesis in translocation renal cell carcinoma. [RNA-seq]

Project description:The oncogenic mechanisms by which TFE3 fusion proteins drive translocation renal cell carcinoma (tRCC) are poorly characterised. Here, we integrated loss and gain of function experiments with multi-omics analyses in tRCC cell lines and patient tumors. High nuclear accumulation of NONO-TFE3 or PRCC-TFE3 fusion proteins promotes their broad binding across the genome, engaging a core set of M/E-box-containing regulatory elements to activate specific gene expression programs as well as promiscuous binding to active promoters to stimulate mRNA synthesis. Within the core program, TFE3 fusions directly regulate genes involved in ferroptosis resistance and oxidative phosphorylation metabolism (OxPhos) increasing functional OxPhos levels. Consequently, human tRCC tumors display high OxPhos scores that persist during their epithelial to mesenchymal transition (EMT). EMT of tRCC tumours was further associated with presence of mesenchymal tRCC cancer cells and myofibroblast cancer-associated fibroblasts (myCAFs) that are both hallmarks of poor prognostic outcomes. We provide unique insights into how broad genomic binding of TFE3 fusion proteins promotes tRCC tumourigenesis by regulating OxPhos and ferroptosis resistance and more generally stimulating RNA synthesis.

2025-02-01 | GSE268092 | GEO

TFE3 fusion proteins drive oxidative metabolism, ferroptosis resistance and general RNA synthesis in translocation renal cell carcinoma. [Cut and Tag/ChIP-seq]

2025-02-01 | GSE268089 | GEO

TFE3 fusion proteins drive oxidative metabolism, ferroptosis resistance and general RNA synthesis in translocation renal cell carcinoma

Project description:TFE3 fusion proteins drive oxidative metabolism, ferroptosis resistance and general RNA synthesis in translocation renal cell carcinoma

| PRJNA1114646 | ENA

TFE3 fusion proteins drive oxidative metabolism, ferroptosis resistance and general RNA synthesis in translocation renal cell carcinoma. [RNA-seq]

Project description:TFE3 fusion proteins drive oxidative metabolism, ferroptosis resistance and general RNA synthesis in translocation renal cell carcinoma. [RNA-seq]

| PRJNA1114647 | ENA

TFE3 Xp11.2 translocation renal cell carcinoma mouse model

Project description:Renal Cell Carcinoma (RCC) associated with Xp11.2 translocation (TFE3-RCC) has been recently defined as a distinct subset of RCC. The Xp11 translocations involve the TFE3 transcription factor and produce chimeric TFE3 proteins retaining the basic helix-loop-helix leucine zipper structure for dimerization. To facilitate the development of molecular-based diagnostic tools and targeted therapies for TFE3-RCC, we generated a translocation RCC mouse model and performed DNA microarray analysis.

2019-04-20 | GSE130072 | GEO

TFE3 fusion proteins drive oxidative metabolism, ferroptosis resistance and general RNA synthesis in translocation renal cell carcinoma

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

2025-02-01 | GSE268093 | GEO

Effects of SFPQ-TFE3 fusion in kidney tubuloids

Project description:The goal of this study was to analyse the effects of the SFPQ-TFE3 fusion by transforming kidney tubuloids with the construct. Samples without the construct (luciferase only) and overexpressing the partner only (TFE3) were also used as controls. Furthermore, transformed organoids were also transferred into mice PDX models to check their tumorigenic potential; tumors derived from the organoids were subsequently used for sequencing.

2025-02-28 | E-MTAB-13901 | biostudies-arrayexpress

TFE3 Xp11.2 translocation renal cell carcinoma mouse model

Project description:TFE3 Xp11.2 translocation renal cell carcinoma mouse model

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TFE3 fusion oncoprotein condensates drive epigenetic reprogramming and cancer progression

Project description:Translocation renal cell carcinoma (tRCC) presents a significant clinical challenge due to its aggressiveness and limited treatment options. This cancer is primarily driven by fusion oncoproteins (FOs) arising from chromosomal rearrangements, yet their role in oncogenesis remains incompletely understood. Here we investigate TFE3 fusion in tRCC, focusing on NONO::TFE3 and SFPQ::TFE3, constituting 30-40% of all TFE3 FOs. We find that TFE3 FOs form liquid-like condensates with heightened transcriptional activity, selectively recruiting active transcription markers to TFE3 target genes and promoting cell proliferation, migration, and drug resistance. The coiled-coil domains (CCD) of NONO and SFPQ are essential for condensate formation, prolonging TFE3 FOs' chromatin binding time and enhancing transcription. We comprehensively investigated the genome-wide recruitment of TFE3 FOs and their CCD-altered variants, uncovering widespread changes in chromatin accessibility and genomic binding specifically at TFE3 and AP-1 regulated loci. We also observe altered H3K27ac deposition at enhancers and super-enhancers notably at pro-growth and stemness markers such as BCL2 and CD44, and identify novel oncogenic target genes of TFE3 FOs. Disruption of condensate formation, resulting from CCD domain alterations in FOs, robustly dysregulates their role in chromatin accessibility, chromatin binding, H3K27ac occupancy, and gene expression. Altogether our integrated analyses underscore the critical functions of TFE3 FO condensates in driving RCC progression, offering pivotal insights for future targeted therapeutic strategies.

2025-04-02 | GSE281477 | GEO

Hexameric VCP/p97 reprograms transcription by organizing enhancers with the ASPSCR1-TFE3 fusion oncoprotein

Project description:Aberrant transcription in alveolar soft part sarcoma (ASPS) is orchestrated by the fusion oncoprotein, ASPSCR1-TFE3, resulting from a gene fusion created by a t(X;17) chromosomal translocation. Proteomic analysis of co-immunoprecipitated ASPSCR1-TFE3 complexes revealed strong enrichment of VCP/p97, an AAA+ ATPase with known segregase function. VCP and ASPSCR1-TFE3 co-distributed across chromatin and were associated with active enhancers, indicated by flanking peaks of H3K27ac that assemble into higher order chromatin structures by HiChIP. Positive and negative genetic experiments with ASPSCR1-TFE3 and VCP demonstrated that they function co-dependently for cancer cell proliferation, colony formation, enhancer activation, chromatin conformation, and transcription. The VCP associating with ASPSCR1-TFE3 was found by native gel and electron microscopy to be assembled into homo-hexamers. Disruption of VCP hexamer assembly or enzymatic function inhibited the transcriptional impact of ASPSCR1-TFE3. Thus, a segregase was found to bind chromatin and assemble into 3-dimensional structures as a co-factor of transcriptional regulation.

2023-11-23 | PXD022515 | Pride

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