Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mitochondrial superoxide dismutase controls metabolic plasticity in pancreatic cancer

ABSTRACT: Reactive oxygen species have been established to play a critical role in pancreatic carcinogenesis. One of the main antioxidant enzymes is mitochondrial superoxide dismutase (Sod2). Sod2 has been shown to affect tumor initiation and metastatic progression in various cancer types. The impact of Sod2 deletion on pancreatic cancer biology and metabolism has so far not been investigated. We therefore generated three individual Sod2 deficient cell lines from murine pancreatic cancer cell lines isolated from KrasG12D mutant mice and analyzed control and knockout lines with RNA-seq.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Henrik Einwächter

PROVIDER: E-MTAB-16320 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Essential Role of Thioredoxin and Glutathione in Pancreas

Project description:Acute pancreatitis (AP) is defined by acute inflammatory injury to the pancreas and oxidative stress has been implicated as a mechanistic driver of disease progression. To delineate the contribution of reactive oxygen species (ROS) detoxification pathways in AP, we employed a genetic model of pancreas-specific deletion of the thioredoxin reductase 1 (Txnrd1) gene, either alone or in conjunction with pharmacological inhibition of glutathione synthesis via buthionine sulfoximine (BSO). AP was induced in these cohorts and in control animals. Pancreatic tissues were harvested at baseline (0 h), 8 h, 24 h, and 7 days post-induction for RNA sequencing to capture dynamic transcriptional programs. This experimental framework was designed to generate in vivo evidence on how modulation of ROS-scavenging systems influences pancreatic injury severity and subsequent repair processes in the context of AP.

2025-08-30 | E-MTAB-15511 | biostudies-arrayexpress

RNA-Seq of explanted murine pancreatic acinar cells

Project description:To investigate the underlying changes during acinar-to-ductal metaplasia, pancreatic acinar cells were isolated from 5 week old KrasG12D-mice. RNA was isolated immediately after isolation (t=0 days) or after 3 days embedded in collagen.

2023-03-02 | E-MTAB-9878 | biostudies-arrayexpress

RNA-seq of mouse cell lines isolated from genetically engineered mouse models of extrahepatic cholangiocarcinoma and pancreatic cancer

Project description:Biliary tract cancer (BTC) ranks among the most lethal human malignancies, thereby representing an unmet clinical need. In this study, we find that the Pdx1-positive extrahepatic biliary epithelium is highly susceptible towards transformation by activated Pik3caH1047R, but completely refractory to oncogenic KrasG12D. Using genome-wide in vivo piggyBac transposon-based forward genetic screening and genetic loss-of-function experiments, we discover important extrahepatic cholangiocarcinoma (ECC) cancer genes and find that PI3K-signaling output strength and repression of the tumor suppressor p27Kip1 are critical context-specific determinants of tumor formation. This contrasts the pancreas, where oncogenic Kras in concert with Trp53 loss of function are key cancer drivers. Notably, inactivation of p27Kip1 permits KrasG12D-driven ECC development, and bypasses oncogene-induced senescence without triggering the Trp53 pathway. These studies provide a mechanistic link between PI3K-signaling, tissue-specific tumor suppressor barriers, and ECC pathogenesis, and present a novel genetic model of autochthonous ECC and genes driving this highly lethal tumor-subtype.

2021-07-05 | E-MTAB-10515 | biostudies-arrayexpress

RNA-Seq of pancreatic tissue from wt, KrasG12D, Pi3kCAH1047R and Mek1dd mice, at 10 weeks and after induction of acute pancreatitis

Project description:To investigate the underlying changes during acinar-to-ductal metaplasia induced by different oncogenes and by acute pancreatitis, pancreatic tissue was isolated from 10 week old control wt, KrasG12D, Pi3kCAH1047R and Mek1dd mice and from mice of the same genotypes after induction of acute pancreatitis.

2024-04-06 | E-MTAB-13946 | biostudies-arrayexpress

RNA-seq of pancreatic mouse tumor cell lines

Project description:KRAS-mutant pancreatic ductal adenocarcinoma (PDAC) is highly immunosuppressive and resistant to targeted therapies, immune checkpoint blockade and engineered T cells. In this study, we performed a systematic high throughput combinatorial drug screen and identified a synergistic interaction between the MEK inhibitor trametinib and the multi-kinase inhibitor nintedanib. Using bulk and single-cell RNA sequencing and immunophenotyping, we show that the combination therapy reprograms the immunosuppressive microenvironment and primes cytotoxic and memory T cells to infiltrate the tumors, thereby sensitizing mesenchymal PDAC to PD-L1 inhibition.

2021-11-29 | E-MTAB-11187 | biostudies-arrayexpress

RNA-Seq of explanted murine pancreatic acinar cells from wt, KrasG12D, Pi3kCAH1047R and Mek1dd mice

Project description:To investigate the underlying changes during acinar-to-ductal metaplasia induced by different factos, pancreatic acinar cells were isolated from 5 week old wt, KrasG12D, Pi3kCAH1047R and Mek1dd mice. Acinar cells from wt mice were treated with medium (control), Tgfa or IL17a. RNA was isolated immediately after isolation (t=0 days) or after 2-3 days embedded in collagen.

2024-05-31 | E-MTAB-11913 | biostudies-arrayexpress

DRUG-seq data of primary human hepatocyte spheroids treated with compounds

Project description:Primary human hepatocytes treated with 40 compounds (3 concentrations, 0.1xCmax, Cmax and 10xCmax) and vehicle for 7 h. Compounds have different degree of drug-induced liver injury concern. Data for Figure 2 in connected publication.

2026-01-16 | E-MTAB-15612 | biostudies-arrayexpress

DRUG-seq data of HepG2 treated with compounds

Project description:HepG2 treated with 40 compounds (3 concentrations, 0.1xCmax, Cmax and 10xCmax) and vehicle for 7 h. Compounds have different degree of drug-induced liver injury concern. Data for Figure 2 in connected publication.

2026-01-16 | E-MTAB-15601 | biostudies-arrayexpress

Inhibition of ketohexokinase C isoform impairs the development of PDAC tumors

Project description:the genetic inactivation of Khk-C enhanced the survival of KPC-driven PDAC model even in absence of high fructose diet. Moreover Khk-C knock out decreased the viability of KPC organoids and cancer cells, the migratory capability of PDAC cells in vitro and the growth of KPC cells in vivo in a cell autonomous manner.

2023-07-07 | E-MTAB-12746 | biostudies-arrayexpress