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Brg1 controls stemness and metastasis of pancreatic cancer through regulating hypoxia pathway (ChIP-seq)

ABSTRACT: Brg1 is a subunit of SWI/SNF chromatin remodeling complex. To clarify the role of Brg1 for the progression and metastasis of pancreatic ductal adenocarcinoma (PDAC), we generated a PDAC mouse model with a dual recombinase system (Brg1 lox/lox; Pdx1-Flp; Kras FSF-G12D; Trp53 frt/frt; Rosa26 FSF-CreERT2) which enabled to ablate Brg1 in established PDAC with tamoxifen treatment. We established cancer cell lines derived from PDAC tumors developed in those mice and investigated the effect of Brg1 ablation on PDAC cell proliferation and metastasis. In order to determine the genes that Brg1 directly regulates, we conducted a chromatin immunoprecipitation coupled with deep sequencing (ChIP-seq) analysis for Brg1 and histone modifications (H3K27ac and H3K27me3) using Brg1 wild type and Brg1-deleted mouse PDAC cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE199610 | GEO | 2022/04/30

REPOSITORIES: GEO

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Brg1 controls stemness and metastasis of pancreatic cancer through regulating hypoxia pathway

Project description:Brg1 is a subunit of SWI/SNF chromatin remodeling complex. To clarify the role of Brg1 for the progression and metastasis of pancreatic ductal adenocarcinoma (PDAC), we generated a PDAC mouse model with a dual recombinase system (Brg1 lox/lox; Pdx1-Flp; Kras FSF-G12D; Trp53 frt/frt; Rosa26 FSF-CreERT2) which enabled to ablate Brg1 in established PDAC with tamoxifen treatment. We established cancer cell lines derived from PDAC tumors developed in those mice and investigated the effect of Brg1 ablation on PDAC cell proliferation and metastasis. In order to determine the genes expression in Brg1-deleted mouse PDAC cells, we conducted a transcriptomic analysis using microarray using Brg1 wild type and Brg1-deleted mouse PDAC cells.

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Project description:A pancreatic ductal adenocarcinoma cell line was isolated from a Pdx1-Flp, FSF-KRasG12D/+, Rosa26-CreERT2/tdEG, Mtor-lox/lox mouse. Cultured cells were treated with 4-Hydroxytamoxifen to induce CreERT2 mediated excision of floxed Exon 3 of Mtor.

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RNA-SEQ analysis of pancreatic ductal adenocarcinoma tumours in Pdx1-Cre;lsl-KRas[G12D] (KC), Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM] (KMC), Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM];c-Myc[fl/+] (KMC-Mycfl/+), and Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM];Zbtb17[fl/fl] mice (KMC-Miz1fl/fl)

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Characterisation of Grem1 wild-type and mutant murine pancreatic tumours

Project description:We performed RNA-seq analysis on Grem1 wild-type and Grem1-deleted pancreatic tumour tissues from Pdx1-Flp;KrasFSF-G12D;Trp53frt/frt (KPF) mice. We compared the transcriptome between these two groups of tumours with the aim to understand their molecular signatures and the relevance to human pancreatic ductal adenocarcinoma subtypes.

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Project description:Global mRNA expression profiles of murine primary PDAC cells following JQ1 or SAHA monotherapy as well as JQ1-SAHA combination therapy were collected using Affymetix mouse whole genome array (Mouse Genome 430A 2.0 Array) . Primary PDAC cells isolated from Ptf1aCre/+;Kras+/LSL-G12D;p53lox/lox (Kras;p53) mice were treated either with JQ1 (100 nM) or SAHA (2000 nM) or vehicle 10% (2-Hydroxypropyl)-β-cyclodextrin (Sigma-Aldrich) or as combination therapy with the indicated dosage for monotherapy. Total RNA isolation was performed after 6 hours of treatment. Primary PDAC cells from Ptf1aCre/+;Kras+/LSL-G12D;p53lox/lox (Kras;p53) mice treated either with JQ1, SAHA, vehicle or JQ1-SAHA combination were analyzed by global gene expression analysis.

2015-09-20 | E-GEOD-64836 | biostudies-arrayexpress

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Project description:mRNA-seq for expression profiling of Myc and Yap1 activated mouse lung tumors and controls. 4 cohorts of lung tumors induced through nasal instillation of Cre/sgRNA(MS2)-encoding lentivirus in mice carrying conditional P53 loss (P53 F/F), oncogenic Kras (Kras LSL-G12D/+), and CRISPRa/SAM construct (Rosa26(LSL-SAM) or YFP reporter (Rosa26(LSL-YFP): 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-SAM) / lenti(CMV-Cre/U6-sgRNA(Myc) (PPKS/M); 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-SAM) / lenti(CMV-Cre/U6-sgRNA(Yap1) (PPKS/Y); 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-SAM) / lenti(CMV-Cre/U6-sgRNA(non-targeted) (PPKS/NT); 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-YFP) / lenti(CMV-Cre/U6-sgRNA(non-targeted) (PPKY/NT)

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RNA-SEQ analysis of KMC murine pancreatic ductal adenocarcinoma (PDAC) cell line upon siRNA depletion of MYC, KRas or Miz1 (aka Zbtb17)

Project description:MYC is varyingly thought to either complement KRAS or to act as a downstream KRAS effector - here we compared the transcriptomic impact of MYC depletion with that of KRas depletion in a cell line derived from PDAC driven by lsl-KRas^G12D + Rosa26-lsl-MYC^DM. A second question addressed related to the mechanism of MYC-dependent transcriptional repression, which in many instances requires MYC binding to Miz1. We therefore included analysis of Miz1-depleted KMC cells in this experiment

2020-03-16 | E-MTAB-8792 | biostudies-arrayexpress

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