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The SWI/SNF Complex Regulates the PRDM Protein Hamlet to Ensure Lineage Directionality in Drosophila Neural Stem Cells

ABSTRACT: Members of the SWI/SNF chromatin-remodeling complex are among the most frequently mutated genes in human cancer. SWI/SNF complex controls self-renewal and differentiation in stem cell lineages but how this function relates to tumorigenesis is currently unclear. Here, we use Drosophila neuroblasts to demonstrate that the SWI/SNF component Osa (ARID1) prevents tumorigenesis in stem cell lineages by ensuring correct unidirectional lineage progression. Our transcriptome anaysis identifies Ham as a key Osa target gene.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE48242 | GEO | 2014/03/13

SECONDARY ACCESSION(S): PRJNA209341

REPOSITORIES: GEO

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The SWI/SNF Complex Regulates the PRDM Protein Hamlet to Ensure Lineage Directionality in Drosophila Neural Stem Cells

Project description:Members of the SWI/SNF chromatin-remodeling complex are among the most frequently mutated genes in human cancer. SWI/SNF complex controls self-renewal and differentiation in stem cell lineages but how this function relates to tumorigenesis is currently unclear. Here, we use Drosophila neuroblasts to demonstrate that the SWI/SNF component Osa (ARID1) prevents tumorigenesis in stem cell lineages by ensuring correct unidirectional lineage progression. Our transcriptome anaysis identifies Ham as a key Osa target gene. comparison of transcriptomes of wild type Drosophila melanogaster larval type II NB lineages (excluding neurons) and osa RNAi type II lineages containing mainly NB-like cells and INPs

2014-03-13 | E-GEOD-48242 | biostudies-arrayexpress

RNAi knock down of SWI-SNF subunits BRM, MOR, SNR1, OSA, PB, BAP170 and ISWI in Drosophila

Project description:RNAi knockdown of SWI-SNF subunits BRM, MOR, SNR1, OSA, PB, BAP170 and ISWI

2007-03-01 | E-TABM-169 | biostudies-arrayexpress

Integrative multi-omic analysis of the SWI/SNF complex defines a new clinical subgroup of lung adenocarcinoma patients

Project description:Mammalian SWI/SNF complexes are ATP-dependent chromatin remodelers composed of varying combinations of subunits that, together, fine-tune transcriptional regulation and genome integrity. SWI/SNF complex subunits have been identified as major targets of mutations in several tumor types suggesting a relevant role in tumorigenesis. However, there is a lack of comprehensive studies of the whole SWI/SNF complex in lung adenocarcinoma (LUAD). Here, we combined genomic, transcriptomic, and proteomic approaches to identify which SWI/SNF subunits are present in lung cells, as well as their mutational status, mRNA levels, and protein levels in LUAD. For these purposes, we combined data from LUAD primary tumors, normal lung and LUAD cell lines, and external LUAD data from The Cancer Genome Atlas. Importantly, we found that mutations in the SWI/SNF complex in LUAD not only present a high incidence but we also observed that only the mutational status of the SWI/SNF complex and not the mutations in any of the top ten LUAD driver genes is associated with poorer overall survival in LUAD patients. Furthermore, we showed that the expression of the SWI/SNF complex in LUAD suffers an overall repression that cannot be explained exclusively by genetic alterations. Based on our findings, we propose that SWI/SNF-mutant LUAD tumors should be considered as a distinct subgroup with practical applications in the prognosis and follow-up of LUAD patients.

2022-04-01 | PXD017397 | Pride

Transcriptional changes in bone marrow cells upon SWI/SNF inhibition [scRNA-seq]

Project description:Despite significant therapeutic potential of SWI/SNF inhibition therapy, the off-tumor effects of SWI/SNF inhibition remain largely unknown. Here, we quantify the effects of the dual SWI/SNF ATPase inhibitor BRM014 on bone marrow cells in mice. We identify lineage-dependent effects on the B and monocyte lineages within the bone marrow.

2023-01-10 | GSE205571 | GEO

siRNA Knockdown of SWI/SNF complex proteins in prostate cancer cell lines

Project description:Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus siRNAs targeting SWI/SNF complex proteins (SMARCA2, SMARCA4, and SMARCB1). Goal was to determine the effect of SWI/SNF knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SWI/SNF-siRNA treated cells. Three SWI/SNF proteins were targeted: SMARCA2, SMARCA4, and SMARB1. Biological replicates: 1 control replicate, 2 treatment replicates per SWI/SNF protein. Technical replicates: 1 replicate per SWI/SNF protein. Cell lines: 22Rv1 and LNCaP.

2013-07-20 | E-GEOD-40384 | biostudies-arrayexpress

Arid1a restrains Kras-dependent changes in acinar cell identity

Project description:Mutations in members of the SWI/SNF chromatin remodeling family are common events in human cancer, but the mechanisms whereby disruption of SWI/SNF components alters tumorigenesis remain poorly understood. To model the effect of loss of function mutations in the SWI/SNF subunit Arid1a in pancreatic ductal adenocarcinoma (PDAC) initiation, we directed shRNA triggered, inducible and reversible suppression of Arid1a to the pancreas of mice in the setting of oncogenic KrasG12D. Arid1a cooperates with Kras in the adult pancreas as postnatal silencing of Arid1a following sustained KrasG12D expression induces rapid and irreversible reprogramming of acinar cells into mucinous PDAC precursor lesions. In contrast, Arid1a silencing during embryogenesis, concurrent with KrasG12D activation, leads to retention of acinar cell fate. Together, our results demonstrate Arid1a as a critical modulator of Kras-dependent changes in acinar cell identity, and underscore an unanticipated influence of timing and genetic context on the effects of SWI/SNF complex alterations in epithelial tumorigenesis.

2018-07-03 | GSE114567 | GEO

Arid1a restrains Kras-dependent changes in acinar cell identity

2018-07-03 | GSE114576 | GEO

SWI/SNF complex mutations promote thyroid tumor progression and resistance to redifferentiation therapy (RNA-seq, Fig2)

Project description:Recurrent mutations in genes encoding subunits of the SWI/SNF chromatin remodeling complex occur commonly in human cancers of different lineages, including advanced thyroid cancers. Thyroid-specific loss of Arid1a, Arid2 or Smarcb1 in mouse BrafV600E-mutant tumors promotes disease progression and decreased survival, associated with lesion-specific effects on chromatin accessibility and differentiation. Swi/Snf loss leads to a repressive chromatin state at thyroid lineage transcription factors and their target binding sites, resulting in impaired expression of genes required for thyroid hormone biosynthesis. Thyroid differentiation and response to radioiodine therapy is restored by MAPK inhibitors in mouse BrafV600E-mutant thyroid cancers, which is abrogated in the context of Swi/Snf loss. MAPK inhibitors also failed to restore thyroid differentiation and radioiodide incorporation in patients with BRAFV600E or RAS-mutant tumors with SWI/SNF mutations. SWI/SNF complexes are central to the maintenance of differentiated thyroid function, and their loss confers RAI refractoriness and resistance to MAPK inhibitor-based redifferentiation therapies.

2020-12-02 | GSE147477 | GEO

SWI/SNF complex mutations promote thyroid tumor progression and resistance to redifferentiation therapy (ATAC-seq, Fig3)

2020-12-02 | GSE147476 | GEO

SWI/SNF complex mutations promote thyroid tumor progression and resistance to redifferentiation therapy (ATAC-seq, Fig2)

2020-12-02 | GSE147475 | GEO