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TRIM33 is an oncogenic transcriptional coactivator stabilizing AR from Skp2-mediated ubiquitin-proteasomal degradation in prostate cancer [RNA-Seq]

ABSTRACT: TRIM33 is an oncogenic transcriptional coactivator stabilizing AR from Skp2-mediated ubiquitin-proteasomal degradation in prostate cancer [RNA-Seq]

PROVIDER: PRJNA730586 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14572115_1.fastq.gz	Fastqsanger.gz
	SRR14572115_2.fastq.gz	Fastqsanger.gz
	SRR14572116_1.fastq.gz	Fastqsanger.gz
	SRR14572116_2.fastq.gz	Fastqsanger.gz
	SRR14572117_1.fastq.gz	Fastqsanger.gz

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TRIM33 is an oncogenic transcriptional coactivator stabilizing AR from Skp2-mediated ubiquitin-proteasomal degradation in prostate cancer [ChIP-seq]

Project description:Using a proteomics approach, we identified the Tripartite Motif Containing 33 (TRIM33) as a novel transcriptional coactivator of AR. We demonstrate TRIM33 facilitates the AR chromatin binding to directly regulate a transcription program that promotes PCa progression by protecting AR from Skp2-mediated ubiquitination and proteasomal degradation. We also show TRIM33 is essential for PCa tumor growth by avoiding cell cycle arrest and apoptosis, and TRIM33 knockdown sensitizes PCa cells to AR antagonists. In clinical analyses, we find TRIM33 is upregulated in multiple PCa patient cohorts. Finally, we uncover an AR-TRIM33 coactivated gene signature that is highly expressed in PCa tumors and predicts disease recurrence. Overall, our results reveal TRIM33 is an oncogenic AR coactivator in PCa and a potential therapeutic target for PCa treatment.

2022-05-05 | GSE174109 | GEO

TRIM33 is an oncogenic transcriptional coactivator stabilizing AR from Skp2-mediated ubiquitin-proteasomal degradation in prostate cancer [RNA-Seq]

2022-05-05 | GSE174589 | GEO

TRIM33 is an oncogenic transcriptional coactivator stabilizing AR from Skp2-mediated ubiquitin-proteasomal degradation in prostate cancer

Project description:TRIM33 is an oncogenic transcriptional coactivator stabilizing AR from Skp2-mediated ubiquitin-proteasomal degradation in prostate cancer

| PRJNA730585 | ENA

TRIM33 is an oncogenic transcriptional coactivator stabilizing AR from Skp2-mediated ubiquitin-proteasomal degradation in prostate cancer [ChIP-seq]

Project description:TRIM33 is an oncogenic transcriptional coactivator stabilizing AR from Skp2-mediated ubiquitin-proteasomal degradation in prostate cancer [ChIP-seq]

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TRIM33 is an oncogenic transcriptional coactivator stabilizing AR from Skp2-mediated ubiquitin-proteasomal degradation in prostate cancer

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

2022-05-05 | GSE174590 | GEO

TRIM33 drives prostate tumor growth by stabilizing androgen receptor from Skp2-mediated degradation.

Project description:Androgen receptor (AR) is a master transcription factor that drives prostate cancer (PCa) development and progression. Alterations in the expression or activity of AR coregulators significantly impact the outcome of the disease. Using a proteomics approach, we identified the tripartite motif-containing 33 (TRIM33) as a novel transcriptional coactivator of AR. We demonstrate that TRIM33 facilitates AR chromatin binding to directly regulate a transcription program that promotes PCa progression. TRIM33 further stabilizes AR by protecting it from Skp2-mediated ubiquitination and proteasomal degradation. We also show that TRIM33 is essential for PCa tumor growth by avoiding cell-cycle arrest and apoptosis, and TRIM33 knockdown sensitizes PCa cells to AR antagonists. In clinical analyses, we find TRIM33 upregulated in multiple PCa patient cohorts. Finally, we uncover an AR-TRIM33-coactivated gene signature highly expressed in PCa tumors and predict disease recurrence. Overall, our results reveal that TRIM33 is an oncogenic AR coactivator in PCa and a potential therapeutic target for PCa treatment.

| S-EPMC9346471 | biostudies-literature

TRIM33 drives prostate tumor growth by stabilizing androgen receptor from Skp2-mediated degradation

Project description:Androgen receptor (AR) is a master transcription factor that drives prostate cancer (PCa) development and progression. Alterations in the expression or activity of AR coregulators significantly impact the outcome of the disease. Using a proteomics approach, we identified the Tripartite Motif Containing 33 (TRIM33) as a novel transcriptional coactivator of AR. We demonstrate that TRIM33 facilitates AR chromatin binding to directly regulate a transcription program that promotes PCa progression. TRIM33 further stabilizes AR by protecting it from Skp2-mediated ubiquitination and proteasomal degradation. We also show that TRIM33 is essential for PCa tumor growth by avoiding cell cycle arrest and apoptosis, and TRIM33 knockdown sensitizes PCa cells to AR antagonists. In clinical analyses, we find TRIM33 upregulated in multiple PCa patient cohorts. Finally, we uncover an AR-TRIM33 coactivated gene signature highly expressed in PCa tumors and predicts disease recurrence. Overall, our results reveal that TRIM33 is an oncogenic AR coactivator in PCa and a potential therapeutic target for PCa treatment.

| S-SCDT-EMBOR-2021-53468-T | biostudies-other

Dynamics of TRIM33 binding in macrophages and effects of TRIM33 deletion on chromatin state during activation of primary macrophages.

Project description:To get insight into TRIM33 functions, TRIM33 ChIP-seq was carried out in murine macrophage cell line (RAW) and in bone marrow-derived macrophages (BMDM). The results showed that, in addition to its role in hematopoietic differentiation, TRIM33 may modulate PU.1 transcriptional activity during macrophage development and/or activation.To characterize the role of TRIM33 in macrophages, we bred TRIM33fl/fl mice with Lyz-Cre mice where the Cre recombinase gene is under the regulatory sequences of the Lyz gene that is expressed only in mature myeloid cells. Bone marrow cells from LyzCre/Trim33+/+ mice and LyzCre/Trim33flox/flox mice were differentiated in macrophages and treated during 0h, 4h, 12h and 24h with LPS. Using ChIP-seq, we provide a link between TRIM33 binding and H3K4me3 spreading on inflammatory genes in macrophages. Chromatin immunoprecipitations of TRIM33 and H3K4Me3 followed by multiparallel sequencing performed in murine bone marrow-derived macrophages (BMDM).

2015-11-23 | E-GEOD-43654 | biostudies-arrayexpress

MDAMB231 transcriptome response to SKP2 knockdown

Project description:The SKP2 was knockdown by siRNAs in MDA-MB231 cells and RNA-Seq was used to define the transcriptome response to SKP2

2020-12-14 | GSE163110 | GEO