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Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation [RNA-Seq]

ABSTRACT: The aim of the study is to identify AR target gens in LNCaP cells 6 samples correponding to 2 times 3 replicates were used for the study

ORGANISM(S): Homo sapiens

SUBMITTER: Eric Metzger

PROVIDER: E-GEOD-64529 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation [ChIP-Seq]

Project description:The aim of the study is to identify AR target gens in LNCaP cells 5 samples corresponding to LSD1 K114me2 or CHD1 genome-binding in DHT-treated and control LNCaP cells. 6 samples corresponding to LSD1 K114me2 or CHD1 genome-binding in LNCaP cells knocked-down for LSD1 or CHD1 and treated with DHT.

2015-12-07 | E-GEOD-64528 | biostudies-arrayexpress

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Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation

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LSD1 complexes - Assembly of methylated KDM1A and CHD1 drives androgen receptor-dependent transcription and translocation

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Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation

Project description:Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation

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GABARAPL1 Promotes AR+ Prostate Cancer Growth by Increasing FL-AR/AR-V Transcription Activity and Nuclear Translocation.

Project description:The next generation Androgen receptor (AR)-targeted therapies are now in widespread clinical use and prolong prostate cancer (CaP) patient survival. However, the therapies are not curative due to diverse range of resistance mechanisms. AR variants (AR-V), one major mechanism of resistance, has recently gained momentum. Here, we found that GABARAPL1 knockdown inhibits the growth of AR-positive LNCaP and CWR22rv1 CaP cells in vitro and in vivo, decreases AR/AR-V transcription activity and AR nuclear translocation. Pulldown assay shows that both of Full-length (FL)-AR and AR-V were able to interact with GABARAPL1, suggesting that GABARAPL1 may play its role through directly scaffolding AR. The further analysis from Oncomine database showed that negative correlation between GABARAPL1 expression and 5-years survival in CaP cases. Our findings have identified GABARAPL1 as critical regulator of FL-AR/AR-V, suggesting the potential benefit of targeting GABARAPL1 to treat AR-positive CaP that is resistant to next generation AR inhibitors.

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Loss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation.

Project description:Metastatic prostate cancer is characterized by recurrent genomic copy number alterations that are presumed to contribute to resistance to hormone therapy. We identified CHD1 loss as a cause of antiandrogen resistance in an in vivo small hairpin RNA (shRNA) screen of 730 genes deleted in prostate cancer. ATAC-seq and RNA-seq analyses showed that CHD1 loss resulted in global changes in open and closed chromatin with associated transcriptomic changes. Integrative analysis of this data, together with CRISPR-based functional screening, identified four transcription factors (NR3C1, POU3F2, NR2F1, and TBX2) that contribute to antiandrogen resistance, with associated activation of non-luminal lineage programs. Thus, CHD1 loss results in chromatin dysregulation, thereby establishing a state of transcriptional plasticity that enables the emergence of antiandrogen resistance through heterogeneous mechanisms.

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Ligand induced dissociation of the AR homodimer precedes AR monomer translocation to the nucleus.

Project description:The androgen receptor (AR) regulates male sexual development. We have now investigated AR homodimerization, hormone-dependent monomerization and nuclear translocation in PC-3 and COS-1 cells, by utilizing mutations associated with the androgen insensitivity syndrome: Pro767Ala, Phe765Leu, Met743Val and Trp742Arg. AR wild type (WT) was expressed as a homodimer in the cytoplasm, while none of these mutants formed homodimers. Unlike AR WT which responded to 1 nM dihydrotestosterone (DHT) to dissociate and translocate into the nucleus, AR Pro767Ala and Phe765Leu mutants remain as the monomer in the cytoplasm. In the crystal structure of the AR LBD homodimer, Pro767 and Phe765 reside closely on a loop that constitutes the dimer interface; their sidechains interact with the Pro767 of the other monomer and with the DHT molecule in the ligand-binding pocket. These observations place Phe765 at a position to facilitate DHT binding to Pro767 and lead to dissociation of the AR homodimer in the cytoplasm. This Pro-Phe Met relay may constitute a structural switch that mediates androgen signaling and is conserved in other steroid hormone receptors.

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