Expression data comparing high serum-binding subline of C10F4 (named C10F4-S) with its parental line, C10F4
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Jun-I Wu
PROVIDER: E-MTAB-6936 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Comparison of L1 high metastatic subline (C10F4) to low metastatic subline (C9F6) and normal lung cells from mouse
2021-02-07 | E-MTAB-6512 | biostudies-arrayexpress
Project description:In this study, we explored the molecular basis of site-specific metastasis of breast cancer to the lungs in a clinically relevant model based on the JygMC(A) cell line. In this dataset, we include expression data from JygMC(A) primary mammary tumors, lung metastases, normal mammary glands and normal lung parenchyma. In total, 28 samples were analyzed. We generated the following pairwise comparisons using Partek Genomic Suite 6.6 (PGS, Version 6.6, Partek Inc.): PT vs. NMG; PT vs. LM; LM vs. NL; LM vs. NMG. Genes with an FDR-adjusted p-value < 0.05 and a fold-change > 2 were selected.
2015-11-02 | E-GEOD-63627 | biostudies-arrayexpress
Project description:Genomic changes in low and highly metastatic A549 cells were analyzed by 500K SNP arrays. A large number of genomic alterations were present in A549 cells but no significant differences were observed between the low or highly metastatic A549 cell lines. We generated a NSCLC line with highly increased propensity to form tumor nodules in murine lungs after intravenous injections. Extravasation and growth at a distant site are important parts of the metastatic process and we regarded these as a surrogate marker for in vivo aggressiveness and potential metastatic capability. A549 lung asdenocarcimona cell line with initially low metastatic potential was used for this purpose; these cells formed multiple small nodules in NOD/SCID mice after first i.v.-injection, round 1 (R1). Removal of tumor nodules from the lungs and subsequent re-injection led to a rapid increase in metastatic capacity. A highly aggressive phenotype which was stable over time was evident after three rounds (R3) of in vivo selection for the A549 cell line.
2013-02-21 | E-GEOD-44549 | biostudies-arrayexpress
Project description:Immune responses against tumor cells depend on T lymphocyte attraction and activity within the tumor microenvironment. Specialized immune-interacting fibroblasts, commonly referred to as fibroblastic reticular cells (FRC), form specialized niches in secondary lymphoid organs, originate from embryonic progenitors and foster T cell activation. FRCs have also been detected in tertiary lymphoid structures (TLS) in tumors, differentiating from cancer associated fibroblasts. However, the identity and differentiation of niche-forming cells that foster intra-tumoral T cell activity have remained elusive. Here, we employed single cell RNA-sequencing of EYFP+ fibroblasts and GP33/34-Tetramer+CD8+ T cells from experimental murine lung cancer and cell fate-mapping analysis, which revealed the ability of FRC subsets in lung tumors to differentiate from progenitors situated in mural and adventitial sites. Ablation of FRC progenitors in Tumor T cell environments (TTEs) of murine lungs led to reduced anti-tumor T cell activity and loss of tumor control during experimental coronavirus vector-based immunotherapy. Collectively, our study defines lung cancer-associated FRC niches and key processes involved in stromal-T cell interaction that could pave the way for improved cancer immunotherapy.
2024-11-19 | E-MTAB-13708 | biostudies-arrayexpress
Project description:Exosomes are small vesicles contain cellular nucleic acids, proteins, lipids and other substances secreted by living cells. The special structure of exosomes makes it possible to protect the inside contents exist in blood stably. Recent researches showed that exosomes are blame for tumor metastatic dissemination, recurrence and malignance, which makes them strong competitors in diagnosis of cancer. The proteomics of exosomes in circulatory system as well as the phosphorylation state of them through different stages of colorectal cancer (CRC) process remain rarely reported. Here we isolate and identify proteins and phosphorylated protein in exosomes from human plasma in healthy donors and different stages of CRC patients by prolonged ultracentrifugation and liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS) analysis. In this study, a total of 462 quantitative proteins were identified, meanwhile, the strategy allowed us to identify 177 quantifiable proteins along with 315 sites. Proteins with notable different levels are verified and fibrinogen chain positive (FGA+) circulating exosomes (crExos) from patients and from mice could identify CRC with excellent sensitivity and specificity while perform very well in early diagnosis of adenomas. According to our findings, FGA+ crExos could serve as a potential non-invasive diagnostic and screening tool to detect early stages of CRC to facilitate possible curative surgical therapy.
2020-05-26 | PXD009490 | Pride
Project description:The ability to modulate immune-inhibitory pathways using checkpoint blockade antibodies such as PD-1, PD-L1, and CTLA-4 represents a significant breakthrough in cancer therapy in recent years. This has driven interest in identifying small-molecule-immunotherapy combinations to increase the proportion of responses. Murine syngeneic models, which have a functional immune system, represent an essential tool for pre-clinical evaluation of new immunotherapies. However, immune response varies widely between models and the translational relevance of each model is not fully understood, making selection of an appropriate pre-clinical model for drug target validation challenging. Utilizing RNAseq transcriptomic profiling, we have characterised the changes in gene regulatory pathways and immune populations in CT26 mice after treatment with the combination of anti-PD-L1 and anti-CTLA-4 antibodies. At day 7 post tumor implant, the pathways analysis of differentially expressed genes indicated an enrichment for migration of leukocytes in response to inflammation and communication between innate and adaptive immune cells. Similarly, analysis of upstream regulators suggested that lipopolysaccharide, IL-1B, TNF, IFNG, and NFKB1A pathways associated with inflammation were activated. At day 14, pathways related T-helper cell signalling pathways were upregulated. In addition, upstream regulators of the lipopolysaccharide and IFNG pathway, as well STAT1 and IL21 pathway were enriched, indicative of innate and adaptive immune response to inflammation.
2020-04-16 | E-MTAB-7777 | biostudies-arrayexpress
Project description:Diffuse-type gastric carcinoma is a poor-prognostic cancer with high expression of transforming growth factor (TGF)-β and thick stromal fibrosis. However, detailed investigations on the roles of TGF-β signaling in diffuse-type gastric carcinoma have not been performed. We generated two diffuse-type gastric carcinoma cell lines, dominant-negative TGF-β type II receptor expressing cells (2MLN-dnTβRII) and GFP-expressing cells (2MLN-GFP). Cells were subcutaneously or orthotopically injected into nude mice. Although dnTβRII did not affect the growth of OCUM-2MLN in vitro, it accelerated the growth of subcutaneously or orthotopically transplanted tumors in vivo. By microarray analysis, we found gene expression of TSP-1, an angiogenic inhibitor, was down-regulated in dnTβRII tumors. This results suggested disruption of TGF-β signaling in diffuse-type gastric carcinoma cells leads to alteration of tumor microenvironment and acceleration of tumor growth. We generated two OCUM-2MLN-derived gastric carcinoma cell lines; 2MLN-dnTβRII, which expresses dominant negative form of TβRII, and control 2MLN-GFP, which expresses GFP. The transplanted tumors of these cell lines were subjected to gene expression analysis with Affymetrix U133 plus2 arrays.
2011-12-30 | E-GEOD-12336 | biostudies-arrayexpress
Project description:The tumor suppressor and deubiquitinase (DUB) BAP1 regulates chromatin-associated processes and is frequently mutated in various malignancies. BAP1 and its drosophila orthologue Calypso assemble DUB complexes with ASXL-1, -2, -3 paralogues and ASX respectively, and these cofactors are required for stimulating their DUB activity. However how the DUB activity of BAP1 is regulated remains largely unknown. Here we show that BAP1 promotes monoubiquitination of ASXLs on the ASXM/DEUBAD domain. ASXL2 monoubiquitination promotes its stability or proteasomal degradation, stimulates BAP1 DUB activity and is required for mammalian cell proliferation. Monoubiquitination of ASXL2 is directly catalyzed by UBE2E family of ubiquitin conjugating enzymes and is regulated by deubiquitination. Monoubiquitination of ASX is regulated by Calypso and is required for drosophila development. We further revealed a switch mechanism that tightly regulate BAP1 function, as a monoubiquitination of BAP1 UCH domain is mutually exclusive with ASXL2 monoubiquitination, thus ensuring highly coordinated DUB-mediated signaling.
2018-09-28 | PXD011124 | Pride
Project description:As a master regulator of chromatin structure and function, the EZH2 lysine methyltransferase orchestrates transcriptional silencing of developmental gene networks. Overexpression of EZH2 is commonly observed in human epithelial cancers, such as non- small cell lung carcinoma (NSCLC), yet definitive demonstration of malignant transformation by deregulated EZH2 has proven elusive. Here, we demonstrate the causal role of EZH2 overexpression in NSCLC with a new genetically-engineered mouse model of lung adenocarcinoma. Deregulated EZH2 silences normal developmental pathways leading to epigenetic transformation independent from canonical growth factor pathway activation. As such, tumors feature a transcriptional program distinct from KRAS- and EGFR-mutant mouse lung cancers, but shared with human lung adenocarcinomas exhibiting high EZH2 expression. To target EZH2-dependent cancers, we developed a novel and potent EZH2 inhibitor that arises from a facile synthesis and possesses improved pharmacologic properties. JQEZ5 promoted the regression of EZH2-driven tumors in vivo, confirming oncogenic addiction to EZH2 in established tumors and providing the rationale for epigenetic therapy in a defined subset of lung cancer. Gene expression analysis of 7 samples, 3 EZH2 OE tumors, 2 EZH2 OE normal lung samples, and 2 WT lung samples
2015-11-01 | E-GEOD-70046 | biostudies-arrayexpress
Project description:This experiment is designed to screen miRNAs that are deregulated during breast cancer metastasis. Comparatively analyzing miRNAs in parental MDA-MB-435 cells and cells obtained from its lung metastases, 23 miRNAs expressed differentially, among which 12 were elevated and 11 were down-regulated. Total RNA were extracted from parental MDA-MB-435 cells and cells obtained from its lung metastases after 30 days inoculation. Two biological replications for each treatment.
2012-07-13 | E-GEOD-39358 | biostudies-arrayexpress