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RNA-seq analysis of TCEAL1 knock down with/without docetaxel treatment to enhance docetaxel efficacy in prostate cancer

ABSTRACT: RNA-seq analysis of TCEAL1 knock down with/without docetaxel treatment to enhance docetaxel efficacy in prostate cancer

PROVIDER: PRJEB40036 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4508070_1.fastq.gz	Fastqsanger.gz
	ERR4508070_2.fastq.gz	Fastqsanger.gz
	ERR4508071_1.fastq.gz	Fastqsanger.gz
	ERR4508071_2.fastq.gz	Fastqsanger.gz
	ERR4508072_1.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of TCEAL1 knock down with/without docetaxel treatment to enhance docetaxel efficacy in prostate cancer

Project description:Docetaxel chemotherapy in metastatic prostate cancer offers only a modest survival benefit due to emerging resistance. This experiment studies effect of TCEAL1 gene knock down with/without docetaxel treatment. The TCEAL1 gene was identified as the top candidate gene in vivo CRISPR/Cas9 screen.

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In vivo CRISPR/Cas9 screen to identify candidate therapeutic gene targets to enhance docetaxel efficacy in prostate cancer

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Project description:RNA-seq analysis of TCEAL1 knock down with/without docetaxel treatment to enhance docetaxel efficacy in prostate cancer

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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

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

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

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CD4 T cell activating neoantigens enhance personalized cancer vaccine efficacy

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