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TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE284522 | GEO | 2025/06/10

REPOSITORIES: GEO

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TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination

Project description:The Androgen Receptor (AR) is a ligand-dependent transcription factor that drives prostate cancer development and progression. Although, a detailed effect on AR biology has been described for a number of interacting proteins, many AR coregulators remain to be characterized in relation to their distinct impact on AR function. Here, we describe TRIM33 as a conserved AR-interactor across multiple prostate cancer cell lines. We observed that TRIM33 and AR share overall chromatin interaction profiles, in which TRIM33 is involved in downstream responsive transcriptomic output. In contrast to prior reports, we show that TRIM33 does not impact AR protein stability, but instead propose a model in which TRIM33 facilitates maximal AR activity by interfering with H2BK120 ubiquitination levels.

2025-06-16 | PXD058914 | Pride

TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination [ChIP-seq]

2025-06-10 | GSE284519 | GEO

TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination [RNA-seq]

2025-06-10 | GSE284520 | GEO

TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination

Project description:TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination

| PRJNA1199459 | ENA

TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination [ChIP-seq]

Project description:TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination [ChIP-seq]

| PRJNA1199461 | ENA

TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination [RNA-seq]

Project description:TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination [RNA-seq]

| PRJNA1199467 | ENA

Regulation of androgen receptor transcriptional activity and specificity by RNF6-induced ubiquitination.

Project description:The androgen receptor (AR) plays a critical role in prostate cancer. We have identified a ubiquitin E3 ligase, RNF6, as an AR-associated protein in a proteomic screen. RNF6 induces AR ubiquitination and promotes AR transcriptional activity. Specific knockdown of RNF6 or mutation of RNF6-induced ubiquitination acceptor sites on AR selectively alters expression of a subset of AR target genes and diminishes recruitment of AR and its coactivators to androgen-responsive elements present in the regulatory region of these genes. Furthermore, RNF6 is overexpressed in hormone-refractory human prostate cancer tissues and required for prostate cancer cell growth under androgen-depleted conditions. Our data suggest that RNF6-induced ubiquitination may regulate AR transcriptional activity and specificity through modulating cofactor recruitment.

| S-EPMC2848969 | biostudies-literature

Identification of a novel K311 ubiquitination site critical for androgen receptor transcriptional activity.

Project description:The androgen receptor (AR) is the main driver of prostate cancer (PC) development and progression, and the primary therapeutic target in PC. To date, two functional ubiquitination sites have been identified on AR, both located in its C-terminal ligand binding domain (LBD). Recent reports highlight the emergence of AR splice variants lacking the LBD that can arise during disease progression and contribute to castrate resistance. Here, we report a novel N-terminal ubiquitination site at lysine 311. Ubiquitination of this site plays a role in AR stability and is critical for its transcriptional activity. Inactivation of this site causes AR to accumulate on chromatin and inactivates its transcriptional function as a consequence of inability to bind to p300. Additionally, mutation at lysine 311 affects cellular transcriptome altering the expression of genes involved in chromatin organization, signaling, adhesion, motility, development and metabolism. Even though this site is present in clinically relevant AR-variants it can only be ubiquitinated in cells when AR retains LBD suggesting a role for AR C-terminus in E2/E3 substrate recognition. We report that as a consequence AR variants lacking the LBD cannot be ubiquitinated in the cellular environment and their protein turnover must be regulated via an alternate pathway.

| S-EPMC5389688 | biostudies-literature

Overexpression of c-Myc antagonises transcriptional output of the androgen receptor in prostate cancer

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

2017-04-14 | GSE73995 | 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.

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