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Transcriptome analysis of isolated stormal cells and tumor epithelial cells in mouse lung cancer by RNA-Seq

ABSTRACT: We sequenced mRNA from individual stormal cells (Macrophages, Monocytes, and Neutrophils) and tumor epithelial cells from KrasG12dD; p53-/- murine lung cancer model and WT control mouse to compare gene expressio profiles of lung cancer stroma and tumor cells to their counterparts of WT lugns. The tumor was generated by injecting HKP1 lung cancer cell line, which was driven by KrasG12D activation and loss of p53, via tail vein. The cells were sorted by their specific surface markers at day 20-25 after orthortopic lung cancer formation. Examination of mRNA levels in individual stormal cells and tumor cells from tumor lungs compared to their counterparts from WT lungs

ORGANISM(S): Mus musculus

SUBMITTER: Hyejin Choi

PROVIDER: E-GEOD-59831 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptome analysis of individual stromal cell populations identifies stroma-tumor crosstalk in mouse lung cancer model.

Choi Hyejin H Sheng Jianting J Gao Dingcheng D Li Fuhai F Durrans Anna A Ryu Seongho S Lee Sharrell B SB Narula Navneet N Rafii Shahin S Elemento Olivier O Altorki Nasser K NK Wong Stephen T C ST Mittal Vivek V

Cell reports 20150219 7

Emerging studies have begun to demonstrate that reprogrammed stromal cells play pivotal roles in tumor growth, metastasis, and resistance to therapy. However, the contribution of stromal cells to non-small-cell lung cancer (NSCLC) has remained underexplored. We used an orthotopic model of Kras-driven NSCLC to systematically dissect the contribution of specific hematopoietic stromal cells in lung cancer. RNA deep-sequencing analysis of individually sorted myeloid lineage and tumor epithelial cell ...[more]

PMID: 25704820

Similar Datasets

Transcriptome analysis of isolated stormal cells and tumor epithelial cells in mouse lung cancer by RNA-Seq

Project description:We sequenced mRNA from individual stormal cells (Macrophages, Monocytes, and Neutrophils) and tumor epithelial cells from KrasG12dD; p53-/- murine lung cancer model and WT control mouse to compare gene expressio profiles of lung cancer stroma and tumor cells to their counterparts of WT lugns. The tumor was generated by injecting HKP1 lung cancer cell line, which was driven by KrasG12D activation and loss of p53, via tail vein. The cells were sorted by their specific surface markers at day 20-25 after orthortopic lung cancer formation.

2015-03-06 | GSE59831 | GEO

Detection of oncoantigens suitable for lung cancer vaccination

Project description:The lung cancer tumor K-rasLA1/ p53 R172HDeltag mouse model was used to identify genes associated to the tumor mass increase in lungs. Those genes were then ranked on the basis of their oncogenic potential using a metadataset encompassing 695 human lung adenocarcinomas and ranking them on the basis of their expression in normal tissues. The genes characterized by the higher oncogenic potential combined to a low expression in normal tissues were selected as putative targets for preclinical studies on lung cancer vaccination. Two prototypic situations (WT, and MUT) were examined using Exon arrays over a three-points time course (10, 20, and 30 weeks old animals), for each time point two/three male and female animals were used. A total of 30 mouse Exon 1.0 arrays were hybridized.

2013-12-30 | E-GEOD-30878 | biostudies-arrayexpress

Transcriptional profiling of lung tumour cell lines with distinct p53 mutations in the absence or presence of WT p53

Project description:Microarray expression data generated to determine the impact of defined p53 mutations on lung cancer cell phenotypes, and on the tumour supressive responses induced by WT p53 restoration. In murine models of lung cancer, the therapeutic benefit of WT p53 restoration has been demonstrated in p53-deficient tumours (Juntilla et al, 2010; Feldser et al, 2010). However, it remains unknown if the restoration of WT p53 function is beneficial in p53 mutant tumours. Thus, to determine the impact of p53-targeted therapy in mutant p53 lung cancer, we analysed cells from murine lung tumours of distinct p53 genotypes. Utilising the well characterised p53-ER allele (Christophorou et al, 2005; Martins et al, 2006; Juntilla et al, 2010) we carried out transcriptional profiling of KrasG12D/+ cell lines isolated from advanced lung tumours with defined p53 status: p53Fx/ER (null), p53R270H/ER and p53R172H/ER in the absence (p53 WT OFF) or presence (p53 WT ON) of 4-hydroxytamoxifen (4-OHT). The temporal specificity of p53-ER restoration allowed us to utilised two timepoints to determine both the immediate (2hr) and sustained (8hr) impact of WT p53 function.

2017-08-09 | GSE94758 | GEO

Detection of oncoantigens suitable for lung cancer vaccination

2013-12-30 | GSE30878 | GEO

Gene expression signatures for murine alveolar type II lung epithelial cells after tumor bearing

Project description:To determine the influence of primary tumors on pre-metastatic lungs, we have employed whole genome microarray expression profiling as a discovery platform to identify gene signatures of alveolar type II epithelial cells (AT-II) in TLR3 deficient mice (Tlr3-/-) and wide-type (WT) littermates with tumor bearing. We subcutaneously inoculated Tlr3-/- and WT mice with Lewis lung carcinoma (LLC). Two weeks later, lung tissues from Tlr3-/- and WT mice were dissociated and AT-II cells were sorted. AT-II cells from mice without tumor bearing were set as controls. Primary tumor induced gene expression in AT-II cells from Tlr3-/- and WT mice was measured at 2 weeks after tumor inoculation subcutaneously. AT-II cells from mice without tumor bearing were set as controls.

2016-08-10 | E-GEOD-76397 | biostudies-arrayexpress

Gene expression signatures for murine alveolar type II lung epithelial cells after tumor bearing

2016-08-10 | GSE76397 | GEO

Expression data from human fetal lung normal diploid fibroblasts

Project description:The interaction between cancer and stroma plays a key role in tumor progression. Inactivation of p53 is often observed in stromal cells surrounding in cancer, suggesting that p53 in fibroblasts is involved in tumor progression. To elucidate the mechanism by which p53 loss in fibroblasts effect on proliferation and invasiveness of cancer cells, we performed comprehensive expression profiling analyses between p53 knockdown and control fibroblasts using GeneChip Human Genome U133 plus 2.0 arrays. Intact human fetal lung normal diploid fibroblasts TIG-7 cells and TIG-7 cells infected with lentiviruses for the expression of shRNA against p53 were used for RNA extraction and hybridization on Affymetrix microarrays.

2014-08-01 | E-GEOD-58753 | biostudies-arrayexpress

Stage-specific sensitivity to p53 restoration in lung cancer

Project description:This SuperSeries is composed of the following subset Series: GSE23873: Stage-specific sensitivity to p53 restoration in lung cancer: cell line data GSE23874: Stage-specific sensitivity to p53 restoration in lung cancer: tumor data Refer to individual Series

2010-11-24 | E-GEOD-23875 | biostudies-arrayexpress

The lung-enriched p53 mutants V157F and R158L/P regulate a novel transcriptome in lung cancer

Project description:Lung cancer is the leading cause of cancer-related deaths in the US, and alterations in the tumor suppressor gene TP53 are the most frequent somatic mutation among all histologic subtypes of lung cancer. Mutations in TP53 frequently result in a protein that exhibits not only loss of tumor suppressor capability but also gain of oncogenic function (GOF). The canonical p53 hotspot mutants R175H and R273H, for example, confer upon tumors a metastatic phenotype in murine models of mutant p53. To our knowledge, GOF phenotypes of the less often studied V157, R158, and A159 mutants – which occur with higher frequency in lung cancer compared with other solid tumors – have not been defined. In this study, we aimed to define whether the lung mutants are simply equivalent to full loss of the p53 locus, or whether they additionally acquire the ability to drive new downstream effector pathways. Using a publicly available human lung cancer dataset, we characterized patients with V157, R158, and A159 p53 mutations. Additionally, we show here that cell lines with mutant p53-V157F, p53-R158L, and p53-R158P exhibit a loss of expression of canonical wildtype p53 target genes. Furthermore, these lung-enriched p53 mutants regulate genes not previously linked to p53 function including PLAU. Paradoxically, mutant p53 represses genes associated with increased cell viability, migration, and invasion. These findings collectively represent the first demonstration that lung-enriched p53 mutations at V157 and R158 regulate a novel transcriptome in human lung cancer cells and may confer de novo function.

2019-09-26 | GSE120534 | GEO

Mutant p53 attenuates the anti-tumorigenic activity of fibroblasts secreted interferon (IFN) beta

Project description:Mutations in the p53 tumor suppressor protein are highly frequent in tumors and often endow cells with tumorigenic capacities. We sought to examine a possible role for mutant p53 in the cross-talk between cancer cells and their surrounding stroma, which is a crucial factor affecting tumor outcome. Here we present a novel model which enables to individually monitor the response of cancer cells and stromal cells (fibroblasts) to co-culturing. We found that fibroblasts elicit the interferon beta (IFNβ) pathway when in contact with cancer cells, thereby inhibiting their migration. Mutant p53 in the tumor was able to alleviate this response via SOCS1 mediated inhibition of STAT1 phosphorylation. IFNβ on the other hand, reduced mutant p53 RNA levels by restricting its RNA stabilizer, WIG1. These data underscore mutant p53 oncogenic properties in the context of the tumor microenvironment and suggest that mutant p53 positive cancer patients might benefit from IFNβ treatment. As we planned to investigate the effect of mutant p53 we chose to work with lung cancer cells (H1299) which are null for p53 expression and introduce them with two p53 ‘hotsopt’ mutations residing within the DNA binding domain namely R175H and R248Q (H1299175 and H1299248 respectively, Figure 1A and B). The cells were then labeled with a red fluorescent protein (dsRed), while lung CAFs (HK3-T) were labeled with a green fluorescent protein (GFP). The labeled populations were co-cultivated for 24 hours and separated by Fluorescence Associated Cell Sorting (FACS) based on their specific fluorescent marker. RNA was extracted and samples were loaded on chips. Samples were loaded against a common reference sample which contained equal amount of RNA from all samples.

2013-10-10 | E-GEOD-41477 | biostudies-arrayexpress

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