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Evaluation of the impact of aging on lung tumor progression

ABSTRACT: To understand the impact of aging on lung tumor progression, we isolated lung tumor cells from Kras LSL-G12D/+; Trp53 fl/fl (KP) mouse models at different stage of tumor progression and performed single-cell sequencing on them.

ORGANISM(S): Mus musculus

PROVIDER: GSE277408 | GEO | 2024/09/19

REPOSITORIES: GEO

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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

mRNA-seq of Myc and Yap1-activated mouse lung tumors and controls

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2022-08-30 | E-MTAB-11122 | biostudies-arrayexpress

CD109 regulates in vivo tumor invasion in lung adenocarcinoma through TGF-β signaling

Project description:CD109 is a glycosylphosphatidylinositol-anchored glycoprotein highly expressed in several types of human malignant tumors including lung cancers. We investigated the in vivo functions of CD109 protein in malignant lung tumors. CD109+/+ and CD109-/- K-ras[LSL-G12D/+];p53[fl/fl] (KP) mice were sacrificed at 20 to 23 weeks of age and total RNA was extracted from the lung tumors. SurePrint G3 Mouse GE Microarray 8×60K Ver.2.0 were performed.

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RIP4 inhibits Interleukin-6 Signaling to sustain Lung Adencarcinoma Differentiation

Project description:Evaluation of the role of RIP4 in lung adenocarcinoma revealed that RIP4 inhibits IL6 mediated STAT3 signaling in vitro and in vivo. Repression of RIP4 enhanced IL6 signaling activation in KRAS LSL/G12D/wt; p53flox/flox murine tumors. This promoted cancer dedifferentiation through ECM remodeling Investigation of transcriptional changes in KP tumors expressing shRNA against RIP4 or p53 (control) by microarray (Mouse gene 2.0 ST array from affymetrix)

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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

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 between mouse UPS tumors (KP) and mouse UPS tumors without HIF-2alpha (KPH2)

Project description:Purpose: determine RNA expression differences in an unbiased fashion between UPS tumors derived from LSL-KrasG12D;Trp53-/- (KP) mice, and UPS tumors derived from LSL-KrasG12D;Trp53-/-;Epas1-/- (KPH2) mice. Epas1 encodes HIF-2alpha protein. RNA-seq was performed on KP (n = 4) and KPH2 (n = 4) derived UPS tumors using Illumina HiSeq 2000.

2015-12-31 | E-GEOD-67672 | biostudies-arrayexpress

Expression data from mouse lung squamous cell carcinoma isolated from KrasG12D;Lkb1 mice treated with Vehicle or with catalytic mTOR inhibitor MLN128 for 8 weeks

Project description:Lung tumors were induced in Kras LSL-G12D; Lkb1 fl/fl mice by intranasal inhalation of Adenoviral Cre. Four weeks after tumor induction, mice were randomly assigned into two groups and treated daily with either Vehicle or 1mg/kg MLN128 for 8 weeks. At the end of the study, mice were euthanized and tumors were dissected out from lung and snap frozen in liquid nitrogen. Frozen tumors were stored in -80C freezer. Lung squamous cell carcinomas adapted to chronic treatement with MLN128 We used microarrays to examine changes in the gene expression in pathways that allowed MLN128 treated squamous cell carcinomas to continue to proliferate in the presence of MLN128

2018-02-06 | GSE110108 | GEO

Epigenomic profiling of Non-small-cell Lung Cancer (NSCLC) cells with or without Eed

Project description:Polycomb repressive complexes (PRC) are frequently implicated in human cancer acting either as oncogenes or tumor suppressors. Here we show that PRC2 is a critical regulator of Kras-driven non-small-cell lung cancer (NSCLC) progression. Modulation of PRC2 by either Ezh2 overexpression or Eed deletion enhances Kras-driven adenomagenesis and inflammation, respectively. Eed-loss-driven inflammation leads to massive macrophage recruitment and marked decline in tissue function. Additional Trp53 inactivation activates a cell autonomous epithelial-to-mesenchymal transition (EMT) program leading to an invasive mucinous adenocarcinoma. A switch between methylated/acetylated chromatin underlies the tumor phenotypic evolution, prominently involving genes controlled by Hippo/Wnt-signaling. Our observations in the mouse models were conserved in human cells. Importantly, PRC2 inactivation results in context-dependent phenotypic alterations, with implications for its therapeutic application. We generated ChIP-seq from primary Kras;p53 (KP) cells in culture with and without Eed (KPE) and from KP primary tumors generated by injection of NSCLC into the tail vein. Mice were sacrificed on the onset of shortness of breath. We generated genome-wide expression profiles (RNA-seq) and Nuclease Accessibility (NA)-seq in primary KP and KPE tumor cells. NA-seq was also performed in A549 cells.

2016-01-15 | E-GEOD-61190 | biostudies-arrayexpress

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: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)

| PRJEB36783 | ENA

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