{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"submitter":["Henrik Einwächter"],"organism":["Mus musculus"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16320"],"description":["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."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Nucleic Acid Extraction - Total RNA of cancer cell lines was isolated using Maxwell® 16 LEV simplyRNA Tissue Kit (AS1280, Promega) and Maxwell® 16 Instrument (Promega) as per manufacturer’s instructions","Library Construction - Library preparation for bulk 3’-sequencing of poly(A)-RNA was done as described previously (Parekh et al., 2016) barcoded cDNA of each sample was generated with a Maxima RT polymerase (Thermo Fisher) using oligo-dT primer containing barcodes, unique molecular identifiers (UMIs) and an adapter. 5’ ends of the cDNAs were extended by a template switch oligo (TSO) and after pooling of all samples full-length cDNA was amplified with primers binding to the TSO-site and the adapter. cDNA was tagmented with the Nextera XT kit (Illumina) and 3’-end-fragments finally amplified using primers with Illumina P5 and P7 overhangs.","Sample Collection - Cells were seeded at a density of 10.000 cells in 6 cm dishes and after attachment, were cultured for 24 hours.","Sequencing - The library was sequenced on a NextSeq 500 (Illumina) with 16 cycles for the barcodes and UMIs in read1 and 65 cycles for the cDNA in read2.","Sample Treatment - Culture in standard medium +/- 60 µM 10058-F4 (Myc Inhibitor)"],"figure_sub":["Organization","MINSEQE Score","Assays and Data","Processed Data","MAGE-TAB Files"],"data_protocol":["Sequence Alignment - Reference genome (GRCm38) was used for alignment. Transcript and gene definitions were used according to the ENSEMBL annotation release 75.","Data Transformation - Data was processed using the published Drop-seq pipeline (v1.0) to generate sample-and gene-wise UMI tables (Macosko et al., 2015). The submitted count files contain raw UMI counts with no normalization applied."],"omics_type":["Unknown","Transcriptomics","Genomics","Proteomics"],"instrument_platform":["NextSeq 500"],"study_type":["RNA-seq of coding RNA"],"species":["Mus musculus"],"pubmed_authors":["Henrik Einwächter"],"additional_accession":[]},"is_claimable":false,"name":"Mitochondrial superoxide dismutase controls metabolic plasticity in pancreatic cancer","description":"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.","dates":{"release":"2025-12-23T00:00:00Z","modification":"2025-12-23T02:02:20.799Z","creation":"2025-11-28T15:15:56.286Z"},"accession":"E-MTAB-16320","cross_references":{"ENA":["ERP185803"],"EFO":["EFO_0002944","EFO_0004170","EFO_0004917","EFO_0005518","EFO_0003816","EFO_0003738","EFO_0004184","EFO_0003969"]}}