Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

54 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Small and large RNA sequencing of a Kras G12D mouse model of lung adenocarcinoma

ABSTRACT: Mice bearing a G12D activating mutation in Kras consistently develop lung adenocarcinomas in a manner analogous to humans. By performing small and large RNA sequencing on KrasG12D tumors from F1 hybrid mice we were able to identify genes and microRNAs differentially expressed in these tumor samples. Quantification of reads that cover single nucleotide polymorphisms that distinguish between the parental mouse strains enabled an analysis of allele specific expression and imprinting status in these tumors. mRNA and small RNA fractions of mouse lungs and lung adenocarcinomas were deep sequenced in triplicate

ORGANISM(S): Mus musculus

SUBMITTER: Paul Valdmanis

PROVIDER: E-GEOD-43028 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Proliferation and Tumorigenesis of a Murine Sarcoma Cell Line in the Absence of Dicer

Project description:MicroRNAs are a class of short ~22 nucleotide RNAs predicted to regulate nearly half of all protein-coding genes, including many involved in basal cellular processes and organismal development. Although both increases and decreases in the levels of specific miRNAs have been shown to promote tumor development, a global reduction in miRNAs is commonly observed in various human tumors. However, complete loss has not been documented, suggesting an essential function for miRNAs in tumorigenesis. Here we present the finding that transformed or immortalized Dicer-null somatic cells can be isolated readily in vitro, maintain the characteristics of Dicer-expressing controls and remain stably proliferative. Furthermore, Dicer-null cells from a sarcoma cell line, though depleted of miRNAs, are competent for tumor formation. Hence, miRNA levels in cancer may be maintained in vivo by a complex stabilizing selection in the intratumoral environment. Small RNAs from tumor cell lines (murine sarcoma KrasG12D, p53 -/-) with and without Dicer (Dicer f/-, Dicer -/-) were analyzed.

2012-08-20 | E-GEOD-34825 | biostudies-arrayexpress

Disruption of STAT3 signaling promotes KRAS induced lung tumorigenesis

Project description:Oncogenic STAT3 functions are known in various malignancies. We found that STAT3 plays an unexpected tumor suppressive role in KRAS-mutant non-small-cell-lung cancer (NSCLC). In mice, tissue-specific inactivation of Stat3 resulted in increased Kras (G12D)-driven NSCLC initiation and malignant progression leading to markedly reduced survival. Clinically, low STAT3 expression levels correlate with poor survival in human lung adenocarcinoma patients with smoking history. Consistently, KRAS-mutant lung tumors showed reduced STAT3 levels. Mechanistically, we show that STAT3 controls NFÎºB-induced IL-8-expression by sequestering NFÎºB in the cytoplasm while IL-8 in turn regulates myeloid tumor infiltration and tumor vascularization thereby promoting tumor progression. These results identify a novel STAT3-NFÎºB-IL-8 axis in KRAS-mutant NSCLC with therapeutic and prognostic relevance WT: Control lung; KRAS: Lung tumors expressing KRAS G12D; KRAS STAT3 KO: Lung tumors expressing KRAS G12D- STAT3 deficient; tumors of four mice pooled per sample

2015-02-05 | E-GEOD-52798 | biostudies-arrayexpress

Expression data comparing KRas(G12D/+);CreT, R26(H1047R/+);KRas(G12D/+);CreT, and MMTV-Neu mouse mammary tumors

Project description:Breast Cancer (BC) has been associated with alterations in signaling through a number of growth factor and hormone regulated pathways. Mouse models for metastatic BC have been developed using oncoproteins that activate PI3K, Stat3 and Ras signaling. To determine the role of each pathway, we analyzed mouse mammary tumor formation when they were activated singly or pairwise. We used microarrays to detect differentially expressed genes in the KRas(G12D/+);CreT and R26(H1047R/+);KRas(G12D/+);CreT tumors Total RNA was extracted from tumors developed by Qiagen RNAeasy kit and hybridized on Affymetrix microarrays.

2015-09-16 | E-GEOD-73073 | biostudies-arrayexpress

SIRT6 suppresses pancreatic cancer through control of Lin28b [ChIP-seq]

Project description:Chromatin remodeling proteins are frequently dysregulated in human cancer, yet little is known about how they control tumorigenesis. Here, we uncover an epigenetic program mediated by the NAD+-dependent histone deacetylase Sirtuin 6 (SIRT6) that is critical for suppression of pancreatic ductal adenocarcinoma (PDAC), one of the most lethal malignancies. SIRT6 inactivation accelerates PDAC progression and metastasis via upregulation of Lin28b, a negative regulator of the let-7 microRNA. SIRT6 loss results in histone hyperacetylation at the Lin28b promoter, Myc recruitment, and pronounced induction of Lin28b and downstream let-7 target genes, HMGA2, IGF2BP1 and IGF2BP3. This epigenetic program defines a distinct subset representing 30-40% of human PDAC, characterized by poor prognosis and an exquisite dependence on Lin28b for tumor growth. Thus, we identify SIRT6 as an important PDAC tumor suppressor, and uncover the Lin28b pathway as a potential therapeutic target in a molecularlydefined PDAC subset. ChIP-Seq experiments to examine H3K56ac histone modifications in murine PDAC cells that are Sirt6 wild type (WT), Sirt6 knock-out (KO), and Sirt6 KO cells engineered to express Sirt6 WT (Sirt6 KO + Sirt6 WT Restored).

2016-04-01 | E-GEOD-79503 | biostudies-arrayexpress

Transcriptional profiling of mouse oesophageal tumours from AhcreERTR26flEYFP/wt LSL Kras+/G12D mice

Project description:To assess the transcriptional profile within tumours AhcreERTR26flEYFP/wt LSL Kras+/G12D animals were treated with diethylnitrosamine for 8 weeks prior to induction of the Kras allele with a single dose of Î²-naphthoflavone (20 mg/kg) and tamoxifen (0.25 mg). Subsequently, animals were treated with Sorafenib for 6 weeks. Gene expression array analysis was performed on 12 squamous cell carcinomas (SCCs) from 4 animals.

2016-07-08 | E-MTAB-4926 | biostudies-arrayexpress

SIRT6 suppresses pancreatic cancer through control of Lin28b

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-04-01 | E-GEOD-79505 | biostudies-arrayexpress

Nkx2.1 represses a latent gastric differentiation program in lung adenocarcinoma

Project description:During cancer evolution, cellular differentiation programs become dysregulated. The transcription factor Nkx2-1 is a master regulator of pulmonary differentiation that is downregulated in poorly differentiated lung adenocarcinoma. Here we use conditional murine genetics to study the fate of lung epithelial cells upon loss of their master cell fate regulator. Nkx2-1 deletion in normal and neoplastic lung causes not only loss of pulmonary identity but also gastric transdifferentiation. Nkx2-1 maintains pulmonary identity by sequestering the Foxa1 transcription factor at lung-specific loci and inhibiting Foxa1 binding to gastrointestinal targets. Murine Nkx2-1-negative lung tumors mimic the mucinous subtype of human lung adenocarcinoma, which also exhibits gastric transdifferentiation. Nkx2-1-negative lung adenocarcinomas are dependent on the gastrointestinal gene Hnf4a for efficient initiation. Thus, loss of Nkx2-1 results in transdifferentiation rather than stable dedifferentiation in vivo, suggesting that inactivation of both active and latent differentiation programs may be required for tumors to reach a primitive, dedifferentiated state. The study was designed to compare the expression profiles of Nkx2-1-positive lung adenocarcinomas with tumors in which Nkx2-1 was deleted at the time of initiation or 6-7 months after initiation.

2013-04-10 | E-GEOD-36473 | biostudies-arrayexpress

Global gene expression profiling of mouse liver tissue samples after treated with various anti-HCV shRNAs

Project description:RNA interference (RNAi) is becoming routine in scientific discovery and treating human disease. However, its applications are hampered by unwanted effects. The RNA-Seq analyses from mouse liver samples expressing various anti-HCV shRNAs show that weak base-pairing in both seed and 3’ regions is required to achieve minimal off-targeting effect. We created nine shRNAs against the HCV genome, and transfected shRNA-expressing plasmids into mouse liver via a hydrodynamic tail vein infusion. A plasmid backbone lacking the shRNA sequence was used as a negative control. After 7 days, mouse liver RNAs were harvested and subject to RNA-Seq analysis (two biological repeats).

2014-10-03 | E-GEOD-55131 | biostudies-arrayexpress

P. aeruginosa PAO1 and ΔodsR (ΔPA2076) strains

Project description:We carried out globlal proteomics analysis on P. aeruginosa PAO1 and ΔodsR (ΔPA2076) strains to determine differences following treatment with OA, 10-HOME, or 7,10-DiHOME oxylipin vs non-treated controls.

2019-02-25 | PXD012256 | Pride

Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach vs. Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach microarray

Project description:We wished to investigate the role of E-cadherin loss in our mouse parietal cell/pre-parietal cell E-cadherin knock-out, p53 knock-out, oncogenic Kras induced model of gastric cancer. As such, we isolated RNA from stomach tissue from our E-cadherin knock-out model (Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)) and our E-cadherin heterozygous model (Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)). We then performed a microarray on this stomach tissue from four independent mice of each genotype. Differentially expressed genes were identified and gene set overlap analysis was used to identify pathways enriched in one model over the other.

2018-05-01 | E-MTAB-5833 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data