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A trimeric USP11-USP7-TCEAL1 complex stabilizes paused RNAPII to sustain oncogenic transcription [RNA-seq]

ABSTRACT: A trimeric USP11-USP7-TCEAL1 complex stabilizes paused RNAPII to sustain oncogenic transcription [RNA-seq]

PROVIDER: PRJNA1141427 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30020900_1.fastq.gz	Fastqsanger.gz
	SRR30020900_2.fastq.gz	Fastqsanger.gz
	SRR30020901_1.fastq.gz	Fastqsanger.gz
	SRR30020901_2.fastq.gz	Fastqsanger.gz
	SRR30020902_1.fastq.gz	Fastqsanger.gz

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A trimeric USP11-USP7-TCEAL1 complex stabilizes paused RNAPII to sustain oncogenic transcription [ChIP-seq]

Project description:During early transcription, RNA polymerase II (RNAPII) undergoes a series of structural transitions controlled by cyclin-dependent kinases. Whether protein ubiquitylation and proteasomal degradation affect the fate of RNAPII at core promoters is less well understood. Here we show that the deubiquitinating enzyme USP11 and its heterodimeric partner USP7 form a trimeric complex with TCEAL1, a member of the poorly understood TCEAL (TCEA/TFIIS-like) protein family. TCEAL1 shares sequence homology with the RNAPII interaction domain of the TCEA/TFIIS elongation factor, which controls the fate of backtracked RNAPII. TCEAL1 stabilizes complexes of USP11 with USP7 and with RNAPII. TCEAL1 is recruited to core promoters upon RNAPII pausing and globally enhances the chromatin association of paused RNAPII. Mechanistically, the USP11/USP7/TCEAL1 complex competes with TFIIS for binding to core promoters and protects RPB8, an essential subunit of RNAPII, from degradation, likely preventing TFIIS-mediated transcript cleavage and RNAPII disassembly. In neuroblastoma and other tumors, TCEAL1-dependent genes define a TGF-beta-dependent gene expression program that is characteristic of mesenchymal and invasive tumor cell types, suggesting that the USP11/USP7/TCEAL1 trimer stabilizes paused RNAPII to support a critical oncogenic gene expression program.

2025-04-25 | GSE273323 | GEO

A trimeric USP11-USP7-TCEAL1 complex stabilizes paused RNAPII to sustain oncogenic transcription [RNA-seq]

2025-04-25 | GSE273322 | GEO

A trimeric USP11-USP7-TCEAL1 complex stabilizes paused RNAPII to sustain oncogenic transcription

Project description:A trimeric USP11-USP7-TCEAL1 complex stabilizes paused RNAPII to sustain oncogenic transcription

| PRJNA1141426 | ENA

A trimeric USP11-USP7-TCEAL1 complex stabilizes paused RNAPII to sustain oncogenic transcription [ChIP-seq]

Project description:A trimeric USP11-USP7-TCEAL1 complex stabilizes paused RNAPII to sustain oncogenic transcription [ChIP-seq]

| PRJNA1141429 | ENA

The USP11/TCEAL1 complex promotes transcription elongation to sustain oncogenic gene expression in neuroblastoma [ChIP-seq II]

Project description:During early transcription, RNA polymerase II (RNAPII) undergoes a series of structural transitions controlled by cyclin-dependent kinases. How protein ubiquitylation and proteasomal degradation control the function of RNAPII is less well understood. Here we show that the deubiquitinating enzyme USP11 forms a complex with TCEAL1, a member of the TFIIS (TCEA)-like protein family. TCEAL1 shares sequence homology with the RNAPII interaction domain of the elongation factor TFIIS, which controls the fate of backtracked RNAPII, and competes with TFIIS for binding to core promoters, potentially preventing excessive backtracking. USP11 protects TCEAL1 from proteasomal degradation and TCEAL1 recruits USP11 to RNAPII. Both USP11 and TCEAL1 promote transcription elongation and maintain expression of RPB8, an essential subunit of all three nuclear RNA polymerases. In neuroblastoma USP11- and TCEAL1-dependent genes define a gene expression program that is characteristic for mesenchymal tumors, which are described to escape from many treatments, suggesting that the USP11/TCEAL1 complex promotes transcription elongation to support a critical oncogenic gene expression program

2025-04-25 | GSE294527 | GEO

The USP11/TCEAL1 complex promotes transcription elongation to sustain oncogenic gene expression in neuroblastoma [RNA-seq II]

2025-04-25 | GSE294526 | GEO

A trimeric USP11-USP7-TCEAL1 complex stabilizes paused RNAPII to sustain oncogenic transcription

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

2025-04-25 | GSE273326 | GEO

The USP11/TCEAL1 complex promotes transcription elongation to sustain oncogenic gene expression in neuroblastoma [RNA-seq II]

Project description:The USP11/TCEAL1 complex promotes transcription elongation to sustain oncogenic gene expression in neuroblastoma [RNA-seq II]

| PRJNA1250445 | ENA

The USP11/TCEAL1 complex promotes transcription elongation to sustain oncogenic gene expression in neuroblastoma [ChIP-seq II]

Project description:The USP11/TCEAL1 complex promotes transcription elongation to sustain oncogenic gene expression in neuroblastoma [ChIP-seq II]

| PRJNA1250447 | ENA

USP11 promotes prostate cancer progression by upregulating AR and c-Myc activity [CUT&RUN]

Project description:Androgen receptor (AR) is a main driver for castration-resistant prostate cancer (CRPC). c-Myc is an oncogene underlying prostate tumorigenesis. Here we find that the deubiquitinase USP11 targets both AR and c-Myc in prostate cancer. USP11 expression was upregulated in metastatic prostate cancer and CRPC. USP11 knockdown significantly inhibited prostate cancer cell growth. Our RNA-seq studies revealed AR and c-Myc as the top transcription factors altered after USP11 knockdown. ChIP-seq analysis showed that either USP11 knockdown or replacement of endogenous USP11 with a catalytic-inactive USP11 mutant significantly decreased chromatin binding by AR and c-Myc. We find that USP11 employs two mechanisms to upregulate AR and c-Myc levels: namely, deubiquitination of AR and c-Myc proteins to increase their stability; deubiquitination of H2A-K119Ub, a repressive histone mark, on promoters of AR and c-Myc genes to increase their transcription. AR and c-Myc re-expression in USP11-knockdown prostate cancer cells partly rescued cell growth defects. Thus, our studies reveal a tumor-promoting role for USP11 in aggressive prostate cancer through upregulation of AR and c-Myc activities and support USP11 as a potential target against prostate cancer.

2024-07-13 | GSE268252 | GEO

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