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BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer

ABSTRACT: BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer

PROVIDER: PRJNA631661 | ENA |

REPOSITORIES: ENA

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BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer

Project description:Deregulation of the chromatin remodeller BRG1 contributes to a wide range of malignancies. In prostate cancer BRG1 is over expressed, however, the underlying function and cellular consequences of this are still being uncovered. Here, we have investigated the role of BRG1 in transcription regulation in prostate cancer. We found that BRG1 is over expressed in both the TCGA prostate cancer cohort as well as a panel of prostate cancer and transformed prostate cell lines. We then utilised a temporal model of BRG1 depletion followed by mRNA-seq to examine changes in gene expression. Surprisingly, we detected a modest overall effect, however, a number of genes associated with proliferation and cell cycle progression were down regulated. We find these genes were in part, co-regulated by AR and FOXA1. Corresponding cell cycle analysis conferred G1 arrest, and altered nuclei morphology with depletion of BRG1. This data provides mechanistic insight into the function of BRG1 in prostate cancer.

2021-02-10 | GSE150252 | GEO

BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer.

Project description: Not available

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YB-1 inhibits proliferation of mesothelioma cells through multiple mechanisms

Project description:YB-1 inhibits proliferation of mesothelioma cells through multiple mechanisms

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Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

2023-02-15 | PXD029647 | Pride

BRG1/SMARCA4 is essential for neuroblastoma cell viability through modulation of cell death and survival pathways

Project description:Neuroblastoma (NB) is a neoplasm of the sympathetic nervous system, and is the most common solid tumor of infancy. NBs are very heterogeneous, with a clinical course ranging from spontaneous regression to resistance to all current forms of treatment. High-risk patients need intense chemotherapy, and only 30-40% will be cured. Relapsed or metastatic tumors acquire multi-drug resistance, raising the need for alternative treatments. Owing to the diverse mechanisms that are responsible of NB chemoresistance, we aimed to target epigenetic factors that control multiple pathways to bypass therapy resistance. We found that the SWI/SNF-related, matrix-associated, actin- dependent regulator of chromatin, subfamily a, member 4 (SMARCA4/BRG1) was consistently upregulated in advanced stages of NB, with high BRG1 levels being indicative of poor outcome. Loss-of-function experiments in vitro and in vivo showed that BRG1 is essential for the proliferation of NB cells. Furthermore, whole genome transcriptome analysis revealed that BRG1 controls the expression of key elements of oncogenic pathways such as PI3K/AKT and BCL2, which offers a promising new combination therapy for high-risk NB Non-silencing control (NSC) or shBRG1 lentiviral vectors were transduced in the Neuroblastoma cell lines SK-N-BE(2) by triplicate. 48h post-infection, total RNA was extracted

2016-03-01 | E-GEOD-74622 | biostudies-arrayexpress

Xist RNA antagonizes the chromatin remodeler, BRG1, from the inactive X chromosome

Project description:The noncoding Xist RNA recruits silencing factors to the inactive X (Xi) and facilitates re-organization of Xi structure. Here, we examine the epigenomic landscape of the Xi and assess how Xist alters chromatin accessibility. Interestingly, Xist deletion propels selective chromatin re-accessibility on the Xi, affecting various Xi regions differentially. Re-accessibility is regulated by BRG1, an ATPase subunit of SWI/SNF chromatin remodeling complex. In vitro, RNA binding inhibits the nucleosome remodeling and ATPase activities of BRG1. In vivo, Xist directly interacts with BRG1 and expels BRG1 from the Xi. Xist ablation leads to a selective return of BRG1 in cis, emanating from pre-existing BRG1 sites that are Xist-free. BRG1's return correlates with cohesin re-binding and restoration of topologically associated domains (TADs), and results in formation of de novo Xi "superloops." Thus, Xist RNA binding inhibits BRG1's nucleosome remodeling activity and results in expulsion of the SWI/SNF complex from the Xi.

2019-01-14 | GSE109395 | GEO

Targeting of SMARCA4 bromodomain selectively inhibits leukemic cell proliferation

Project description:Targeting of SMARCA4 bromodomain selectively inhibits leukemic cell proliferation

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Brg1 promotes both tumor suppressive and oncogenic activities at distinct stages of Pancreatic cancer formation

Project description:Pancreatic Ductal Adenocarcinoma (PDA) develops predominantly through pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasm (IPMN) precursor lesions. Pancreatic acinar cells are reprogrammed to a “ductal like” state during PanIN-PDA formation. Here, we demonstrate a parallel mechanism operative in mature duct cells where they undergo “ductal retrogression” to form IPMN-PDA. Brg1, a catalytic subunit of the SWI/SNF complexes, plays a critical antagonistic role in IPMN-PDA development. In mature duct cells Brg1 inhibits the dedifferentiation that precedes neoplastic transformation, thus attenuating tumor initiation. In contrast, Brg1 promotes tumorigenesis in full-blown PDA by supporting a mesenchymal-like transcriptional landscape. We have exploited this duality of Brg1 functions to develop a novel therapeutic approach using an epigenetic drug JQ1. In summary, this study demonstrates the context-dependent roles of Brg1 and points to potential therapeutic treatment options based on epigenetic regulation in PDA. Duct cells were isolated from mice of 3 different genotypes and duct cells from 3 mice of each genotype were sequenced. For the put back experiments, control retrovirus and that expressing Brg1 were transdcued in Brg1 null IPMN mouse cell line.

2015-07-29 | E-GEOD-65315 | biostudies-arrayexpress

YB-1 Knockdown Inhibits the Proliferation of Mesothelioma Cells through Multiple Mechanisms.

Project description: Not available

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Knock down of Ifitm3 inhibits the adult retinal progenitor cell proliferation

Project description:Knock down of Ifitm3 inhibits the mouse adult retinal progenitor cell proliferation.

2022-04-06 | GSE176472 | GEO