E-GEOD-43306
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA185392PRJNA205399PRJNA185391
PROVIDER: E-GEOD-43306 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-43306-analysis-methods.tsv | Tabular | |||
| E-GEOD-43306-analytics.tsv | Tabular | |||
| E-GEOD-43306-analytics.tsv.undecorated | Tabular | |||
| E-GEOD-43306-analytics.tsv.undecorated.unrounded | Tabular | |||
| E-GEOD-43306-analytics.tsv.unrounded | Tabular |
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Similar Datasets
Project description:This model is based on:
Computational Modeling of the Crosstalk Between Macrophage Polarization and Tumor Cell Plasticity in the Tumor Microenvironment.
Abstract:
Tumor microenvironments contain multiple cell types interacting among one another via different signaling pathways. Furthermore, both cancer cells and different immune cells can display phenotypic plasticity in response to these communicating signals, thereby leading to complex spatiotemporal patterns that can impact therapeutic response. Here, we investigate the crosstalk between cancer cells and macrophages in a tumor microenvironment through in silico (computational) co-culture models. In particular, we investigate how macrophages of different polarization (M1 vs. M2) can interact with epithelial-mesenchymal plasticity of cancer cells, and conversely, how cancer cells exhibiting different phenotypes (epithelial vs. mesenchymal) can influence the polarization of macrophages. Based on interactions documented in the literature, an interaction network of cancer cells and macrophages is constructed. The steady states of the network are then analyzed. Various interactions were removed or added into the constructed-network to test the functions of those interactions. Also, parameters in the mathematical models were varied to explore their effects on the steady states of the network. In general, the interactions between cancer cells and macrophages can give rise to multiple stable steady-states for a given set of parameters and each steady state is stable against perturbations. Importantly, we show that the system can often reach one type of stable steady states where cancer cells go extinct. Our results may help inform efficient therapeutic strategies.
2019-09-23 | MODEL1909230002 | BioModels
Project description:<p>Glioblastoma (GBM) is a common and deadly form of brain tumor in adults. Dysregulated metabolism in GBM offers an opportunity to deploy metabolic interventions as precise therapeutic strategies. To identify the molecular drivers and the modalities by which different molecular subgroups of GBM exploit metabolic rewiring to sustain tumor progression, we interrogated the transcriptome, the metabolome, and the glycoproteome of human subgroup-specific GBM sphere-forming cells (GSC). L-fucose abundance and core fucosylation activation were elevated in mesenchymal (MES) compared with proneural GSCs; this pattern was retained in subgroup-specific xenografts and in subgroup-affiliated human patient samples. Genetic and pharmacological inhibition of core fucosylation significantly reduced tumor growth in MES GBM preclinical models. Liquid chromatography-mass spectrometry (LC-MS)-based glycoproteomic screening indicated that most MES-restricted core-fucosylated proteins are involved in therapeutically relevant GBM pathological processes, such as extracellular matrix interaction, cell adhesion, and integrin-mediated signaling. Selective L-fucose accumulation in MES GBMs was observed using preclinical minimally invasive PET, implicating this metabolite as a potential subgroup-restricted biomarker.Overall, these findings indicate that L-fucose pathway activation in MES GBM is a subgroup-specific dependency that could provide diagnostic markers and actionable therapeutic targets.</p><h4><strong>SIGNIFICANCE: </strong>Metabolic characterization of subgroup-specific glioblastoma (GBM) sphere-forming cells identifies the L-fucose pathway as a vulnerability restricted to mesenchymal GBM, disclosing a potential precision medicine strategy for targeting cancer metabolism.</h4><p><br></p><p><strong>Stem cell and cell line assays</strong> are reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS4708' rel='noopener noreferrer' target='_blank'><strong>MTBLS4708</strong></a>.</p><p><strong>Xenograft assays</strong> are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS730' rel='noopener noreferrer' target='_blank'><strong>MTBLS730</strong></a>.</p>
2022-11-08 | MTBLS4708 | MetaboLights
Project description:<p>Glioblastoma (GBM) is a common and deadly form of brain tumor in adults. Dysregulated metabolism in GBM offers an opportunity to deploy metabolic interventions as precise therapeutic strategies. To identify the molecular drivers and the modalities by which different molecular subgroups of GBM exploit metabolic rewiring to sustain tumor progression, we interrogated the transcriptome, the metabolome, and the glycoproteome of human subgroup-specific GBM sphere-forming cells (GSC). L-fucose abundance and core fucosylation activation were elevated in mesenchymal (MES) compared with proneural GSCs; this pattern was retained in subgroup-specific xenografts and in subgroup-affiliated human patient samples. Genetic and pharmacological inhibition of core fucosylation significantly reduced tumor growth in MES GBM preclinical models. Liquid chromatography-mass spectrometry (LC-MS)-based glycoproteomic screening indicated that most MES-restricted core-fucosylated proteins are involved in therapeutically relevant GBM pathological processes, such as extracellular matrix interaction, cell adhesion, and integrin-mediated signaling. Selective L-fucose accumulation in MES GBMs was observed using preclinical minimally invasive PET, implicating this metabolite as a potential subgroup-restricted biomarker.Overall, these findings indicate that L-fucose pathway activation in MES GBM is a subgroup-specific dependency that could provide diagnostic markers and actionable therapeutic targets.</p><h4><strong>SIGNIFICANCE: </strong>Metabolic characterization of subgroup-specific glioblastoma (GBM) sphere-forming cells identifies the L-fucose pathway as a vulnerability restricted to mesenchymal GBM, disclosing a potential precision medicine strategy for targeting cancer metabolism.</h4><p><br></p><p><strong>Xenograft assays</strong> are reported in the current study <strong>MTBLS730</strong>.</p><p><strong>Stem cell and cell line assays</strong> are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4708' rel='noopener noreferrer' target='_blank'><strong>MTBLS4708</strong></a>.</p>
2022-11-08 | MTBLS730 | MetaboLights
Project description:Translating transcriptome of cancer cells in situ in mesenchymal-rich tumor microenvironment
| PRJNA185392 | ENA
Project description:Growing evidence indicates that tumor-associated stroma plays a negative role in human colorectal cancer (CRC). Nature of specific stromal cell populations involved and mechanisms underlying their negative impact remain to be fully understood. In this study we describe the expansion from human primary CRCs of a mesenchymal cell population, referred to as tumor-associated stromal cells (TASCs), resembling bone marrow-derived mesenchymal stem cells (BM-MSCs) in morphology, phenotypes and differentiation potential. We found that, upon co-culture with tumor cells, TASCs acquire membrane-bound TGF-mbTGF-expression, a phenomenon mediated by v6 integrin. MbTGF-expression proved to be critical for triggering epithelial-to-mesenchymal transition (EMT) in tumor cells, eventually leading to enhanced dissemination of circulating tumor cells and increased metastasis formation, in an orthotopic mouse model. Our data identify CRC-associated mesenchymal stem-like cells as critical EMT initiators and suggest mbTGF- as potential novel therapeutic target.
2022-05-19 | PXD005796 | Pride
Project description:Epithelial to Mesenchymal Transition (EMT) has been associated with cancer cell heterogeneity, plasticity and metastasis. It has been the subject of several modeling effort. This logical model of the EMT cellular network aims to assess microenvironmental signals controlling cancer-associated phenotypes amid the EMT continuum. Its outcomes relate to the qualitative degrees of cell adhesions by adherent junctions and focal adhesions, two features affected during EMT. Model attractors recover epithelial, mesenchymal and hybrid phenotypes, and simulations show that hybrid phenotypes may arise through independent molecular paths, involving stringent extrinsic signals.
Of particular interest, model predictions and their experimental validations indicated that: 1) ECM stiffening is a prerequisite for cells overactivating FAK-SRC to upregulate SNAIL1 and acquire a mesenchymal phenotype, and 2) FAK-SRC inhibition of cell-cell contacts through the Receptor Protein Tyrosine Phosphates kappa leads to the acquisition of a full mesenchymal rather than a hybrid phenotype.
2020-06-30 | MODEL2004040001 | BioModels
Project description:By applying RNA-ISH and RNAseq to circulating tumor cells (CTCs), the study provides definitive evidence of epithelial to mesenchymal transition (EMT) across all histological types of breast cancer, identifying mediators such as FOXC1 and TGF-β signaling, and demonstrating dynamic treatment-associated changes in EMT within clusters of CTCs. Epithelial to mesenchymal transition (EMT) has been postulated to contribute to the migration and dissemination of cancer cells, but supporting histopathological evidence is limited. We used a microfluidic device to isolate circulating tumor cells (CTCs), combined with multiplex fluorescent RNA-in-situ hybridization (ISH) and RNA sequencing, to quantify and characterize EMT in breast cancer cells within the bloodstream. Whereas only rare (0.1-10%) cells in the primary tumor expressed both mesenchymal and epithelial markers, such biphenotypic as well as purely mesenchymal cells were enriched among CTCs, across all histological subtypes of breast cancer. In an index patient followed longitudinally, fluctuation in epithelial and mesenchymal states was observed as a function of initial response and subsequent resistance to therapy. Mesenchymal markers were predominant in clusters of tumor cells, many of which had adherent platelets. Finally, RNA sequencing of CTC clusters identified TGF-β and other EMT-related signatures, which were absent from more epithelial CTCs. FOXC1, a known regulator of EMT, was abundantly expressed in mesenchymal CTCs and was detectable within localized regions of the primary breast tumor. Together, these data support a role for EMT in the blood-borne dissemination of breast cancer and point to the dynamic nature of this cell fate change.
2013-02-01 | E-GEOD-41245 | biostudies-arrayexpress
Project description:Transcriptional profiling of liver cancer associated mesenchymal stem cells comparing normal mesenchymal stem cells from adjacent tumor-free tissues of the same patient 8, Goal was to determine to detect the paracrine trophic factors from liver cancer mesenchymal stem cells. 8 represents liver cancer associated MSCs, N8 represents liver normal MSCs Two-condition experiment, 8 vs. N8 cells. Biological replicates: 1 replicate from the same patient.
2012-11-17 | E-GEOD-42357 | biostudies-arrayexpress
Project description:We focus on cancer-associated fibroblasts (CAFs) as an active component of the tumor microenvironment. The transcriptome profiling and analysis of CAFs isolated from breast cancer skin metastasis, cutaneous basal cell carcinoma and squamous cell carcinoma arising from oral cavity mucous membrane unravelled major gene candidates such as the IL-6, VEGF-A and MFGE8 that induced the expression of several markers associated with poor prognosis and epithelial-to-mesenchymal transition in co-cultivated EM-G3 breast cancer cells.
2023-10-02 | E-MTAB-12994 | biostudies-arrayexpress
Project description:A cell line representative of human high-grade serous ovarian cancer (HGSOC) should not only resemble its tumor of origin at the molecular level, but also demonstrate functional utility in pre-clinical investigations. Here we report the integrated proteomic analysis of 26 ovarian cancer cell lines, HGSOC tumors, immortalized ovarian surface epithelial cells, and fallopian tube epithelial cells via a single-run mass spectrometric workflow. The in-depth quantitation of > 10,000 proteins results in three distinct cell line categories: epithelial (group I), clear cell (group II), and mesenchymal (group III). We identify a 67-protein cell line signature, which separates our entire proteomic dataset, as well as a confirmatory publicly available CPTAC/TCGA tumor proteome dataset, into a predominantly epithelial and mesenchymal HGSOC tumor cluster. This proteomics-based epithelial/mesenchymal stratification of cell lines and human tumors indicates a possible origin of HGSOC either from the fallopian tube or from the ovarian surface epithelium.
2017-03-30 | MSV000080814 | MassIVE