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E-MTAB-8792

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

PROVIDER: E-MTAB-8792 | ExpressionAtlas | 2020-12-09

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-8792-analysis-methods.tsv	Tabular
	E-MTAB-8792-analytics.tsv	Tabular
	E-MTAB-8792-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-8792-configuration.xml	Xml
	E-MTAB-8792-g4_g1-mvaPlot.png	Other

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Similar Datasets

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)

Project description:Activation of endogenously expressed KRas[G12D] in the pancreas of mice gives rise primarily to early stage PanIN lesions, however such lesions can occasionally progress to end-stage ductal adenocarcinoma (PDAC). Progression of KRas[G12D]- initiated lesions to PDAC is accelerated by modest expression of MYC from the Rosa26 locus. Deletion of 1 copy of endogenous c-Myc or both copies of endogenous Zbtb17 (aka Miz1), slows progression to PDAC and extends healthful survival of Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM] (KMC) mice. Tumours were removed from mice with all 4 genotypes and validated by histological examination prior to RNA-SEQ analysis.

2020-03-16 | E-MTAB-8797 | biostudies-arrayexpress

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

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

| PRJEB36758 | ENA

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

Analysis of Nucleolin depletion impact on the KRAS-induced proteomic changes in mouse Pancreatic ductal adenocarcinoma cells.

Project description:To reveal the role of Nuclelin (Ncl) downstream of mutant KRAS in shaping the proteome of Pancreatic Ductal Adenocarcinoma (PDAC) cells, we carried out a quantitative proteomics analysis of tumour cells isolated from an inducible mouse model of PDAC (iKras PDAC) (Ying et al., 2012). In this model, oncogenic Kras (G12D) expression can be controlled by administration of doxycycline (Dox). Tandem Mass Tagging (TMT) was employed for quantitative analysis of Dox induced (24hrs) vs. non-induced iKras-PDAC cells, from control or Nucleolin depleted settings. Two independent siRNA oligos were used against Ncl. All samples barcoded and pooled together using TMT 6plex labelling kit (Thermo).

2023-02-12 | PXD038338 | Pride

E-MTAB-3823

Project description:Transcription profiling by 3'-end sequencing of whole blood from pancreatic ductal adenocarcinoma (PDAC) patients and healthy controls for PDAC diagnosis

2025-01-23 | E-MTAB-3823 | ExpressionAtlas

Gene expression analysis between the pancreatic tissues of Pdx1-cre;Kras LSL-G12D and Pdx-cre;KrasLSL-G12D;IKK2/beta F/F mice

2012-01-24 | GSE33322 | GEO

Stromal-derived NRG1 enables oncogenic KRAS bypass in pancreas cancer

Project description:Activating KRAS mutations (KRAS*) in pancreatic ductal adenocarcinoma (PDAC) drive anabolic metabolism and support tumor maintenance. KRAS* inhibitors show initial anti-tumor activity followed by recurrence due to cancer cell intrinsic and immune mediated paracrine mechanisms. Here, we explored the potential role of cancer associated fibroblasts (CAFs) in enabling KRAS* bypass and identified CAF-derived NRG1 activation of cancer cell ERBB2/ERBB3 receptor tyrosine kinases as a mechanism by which KRAS* independent growth is supported. Genetic extinction or pharmacological inhibition of KRAS* resulted in upregulation of ERBB2 and ERBB3 expression in human and murine models, which prompted cancer cell utilization of CAF-derived NRG1 as a survival factor. Genetic depletion or pharmacological inhibition of ERBB2/ERBB3 or NRG1 abolished KRAS* bypass and synergized with KRASG12D inhibitor in combination treatments in mouse and human PDAC models. Thus, we found that CAFs can contribute to KRAS* inhibitor therapy resistance via paracrine mechanisms, providing an actionable therapeutic strategy to improve the effectiveness of KRAS* inhibitors in PDAC patients.

2023-09-22 | GSE240232 | GEO

LC-MS/MS analysis of differential proteins in KRAS-mutant tissues

Project description:86%–90% of pancreatic ductal adenocarcinoma (PDAC) harbor activating mutations in KRAS, which regulate multiple carcinogenic signaling pathways. In order to elucidate the mechanisms underlying KRAS mutation-driven development and progression of PDAC, quantitative proteomics mass-spectrometry(MS) analysis of differential proteins in KRAS-mutant tissues was performed.

2024-11-29 | PXD058402 |

Differential gene expression in Fosl1 siRNA vs Control siRNA treated murine pancreatic cancer cells

Project description:A subset of human pancreatic ductal adenocarcinoma cells (PDACs) is characterized by high Fosl1 expression and Fosl1 is linked to the control of pro-inflammatory pathways and growth of PDAC cells. To mimick the human disease in mice (> 90% of PDAC patients harbour Kras mutations) the mutated LSL-KrasG12D allele was combined with the pancreas specific Cre recombinase Ptf1aCre (p48Cre). The two pancreatic cancer cell lines (Ptf1aCre, LSL-KrasG12D/+) were isolated from these mice and used for transcriptomics studies. The two different murine pancreatic cancer cell lines (Ptf1aCre, LSL-KrasG12D) were treated with two different Fosl1 siRNAs and one control siRNA, each. 72h after transfection a sufficient knockdown was tested by immunoblotting and qPCR. Total mRNA was isolated and checked for integrity. According to manufacture's recommendation the samples were subjected to microarray analysis using the Affymetrix Mouse Gene ST 1.0 array chip to discover differentially expressed genes.

2016-12-23 | E-MTAB-4299 | biostudies-arrayexpress

Gene expression analysis between the pancreatic tissues of Pdx1-cre;Kras LSL-G12D and Pdx-cre;KrasLSL-G12D;IKK2/beta F/F mice

Project description:Constitutive Kras and NF-kB activation is identified as signature alterations in human pancreatic ductal adenocarcinoma (PDAC). Here, we report that pancreas-targeted IKK2/beta inactivation inhibited NF-kB activation and completely suppressed PDAC development. Our findings demonstrated that NF-kB is required for development of pancreatic ductal adenocarcinoma that was initiated by Kras activation. Pancreatic tissue from 4 groups of mice were used in this project: (1) the pancreas normal appearance of Pdx1-cre;KrasLSL-G12D;IKK2/beta mice, (2) the normal pancreas of Pdx1-cre;KrasLSL-G12D mice, (3) the pancreatic lesion of pancreatic intraepithelial neoplasia (PanIN) of Pdx1-cre;KrasLSL-G12D mice, and (4) the pancreatic lesion of PDAC of Pdx1-cre;KrasLSL-G12D mice. Each group included three mice. RNA samples from mouse pancreas were hybridized on GeneChip Mouse Gene 1.0 ST arrays (Affymetrix). Group (1) and group (2) were compared, and group (2), group (3) and group (4) were compared.

2012-01-24 | E-GEOD-33322 | biostudies-arrayexpress

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