S100A4+ Stromal Cells from Normal Lung vs. Metastatic Lung
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE31711 | GEO | 2011/08/30
SECONDARY ACCESSION(S): PRJNA145457
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of S100A4+ stromal cells at the gene expression level in physiological setting versus metastatic setting. Total RNA was isolated from FACS-sorted S100A4+ stromal cells from normal lung of S100A4-GFP transgenic mice compared to FACS-sorted S100A4+ stromal cells from metastatic lung of 4T1 tumor-bearing S100A4-GFP transgenic mice.
2011-08-29 | E-GEOD-31711 | biostudies-arrayexpress
Project description:S100A4 is a known metastasis-promoting factor, rich in the tumor microenvironment. To clarify how extracellular S100A4 execute its pro-metastatic function, we analyzed gene expression in melanoma cells stimulated with recombinant protein rS100A4 and compared it to the expression in control non-stimulated cells. Two melanoma cell lines representing two distinct phenotypes M-bM-^@M-^S invasive (Melmet 1) and non-invasive/proliferative (Melmet 5) M-bM-^@M-^S were included in the study. The response at the gene expression level was much stronger in Melmet 5 than in Melmet 1. Melmet 5 down-regulated genes associated with melanocytic differentiation, indicating that Melmet 5 cells gained dedifferentiated, more invasive phenotype after stimulation with rS100A4. The observed changes in the expression of metabolism associated genes suggested the occurrence of metabolic reprogramming. We conclude that extracellular S100A4 stimulate the transition to the invasive phenotype in poorly-invasive melanoma cells, and that this transition is associated with metabolic reprogrammingve Total RNA was isolated from Melmet 1 and Melmet 5 cells stimulated with rS100A4 protein for 48hrs compared to non-stimulated cells.
2015-02-13 | E-GEOD-65897 | biostudies-arrayexpress
Project description:S100A4 is a known metastasis-promoting factor, rich in the tumor microenvironment. To clarify how extracellular S100A4 execute its pro-metastatic function, we analyzed gene expression in melanoma cells stimulated with recombinant protein rS100A4 and compared it to the expression in control non-stimulated cells. Two melanoma cell lines representing two distinct phenotypes – invasive (Melmet 1) and non-invasive/proliferative (Melmet 5) – were included in the study. The response at the gene expression level was much stronger in Melmet 5 than in Melmet 1. Melmet 5 down-regulated genes associated with melanocytic differentiation, indicating that Melmet 5 cells gained dedifferentiated, more invasive phenotype after stimulation with rS100A4. The observed changes in the expression of metabolism associated genes suggested the occurrence of metabolic reprogramming. We conclude that extracellular S100A4 stimulate the transition to the invasive phenotype in poorly-invasive melanoma cells, and that this transition is associated with metabolic reprogrammingve
2015-02-13 | GSE65897 | GEO
Project description:Nicotinamide N-methyltransferase promotes metastatic colonisation via cancer cell stromal mimicry.
2023-04-24 | PXD027964 | Pride
Project description:Deciphering stromal changes between metastatic and non-metastatic canine mammary carcinomas
| PRJEB57447 | ENA
Project description:Progressive loss of effector functions, especially IFN-γ secreting capability, in effector memory CD8+ T (CD8+ TEM) cells plays a causal role in asthma worsening. However, the mechanisms of CD8+ TEM cell dysfunction remain elusive. Here, we report that S100A4 drives CD8+ TEM cell dysfunction, impairing their protective memory response and promoting asthma worsening in OVA-induced asthma model. We find that allergic CD8+ TEM cells contain two subsets based on S100A4 expression. S100A4+ subsets exhibit dysfunctional effector phenotypes with increased proliferative capability, whereas S100A4- subsets retain effector function but are more inclined to apoptosis, giving rise a dysfunctional CD8+ TEM cell pool. Mechanistically, S100A4 upregulation of mitochondrial metabolism results in a decrease of acetyl-CoA levels, which impair the transcription of effector genes, especially ifn-γ, facilitating cell survival, tolerance and memory potential. Our findings thus reveal general insights into how S100A4 reprograms CD8+ TEM cells into dysfunctional and less protective phenotypes to promote asthma worsening.
2022-03-11 | GSE162116 | GEO
Project description:To identify gene products expressed in S100A4-producing cells in Peyer's patches, we used transgenic mice expressing enhanced green fluorescent protein (EGFP) under the control of the mouse S100A4 promoter (S100A4-GFP mice) and analyzed gene expression profiles using microarray. As a result, we found that S100A4-producing cells expressed many genes characteristic of LysoMac/DCs and ILC3s.
2019-10-22 | GSE127686 | GEO
Project description:The lipid-metabolism up-regulation-mediated M2 polarization provides tumor-associated macrophages (TAMs) with protumor phenotypes during tumor development and progression. However, how TAMs reprogram their lipid-metabolism responding to M2 activators remains unclear. Here, we report that S100A4 is a determinant of macrophage M2 polarization. We find that the growth of carcinoma grafts was impaired in myeloid S100A4-deficient mice. Coincidentally, ablating S100A4 in macrophages reduced their capability of macrophage into utilization utilize of exogenous fatty acids as their major energy source for oxidation. Mechanistic analysis demonstrates that the induction of PPAR-γ responding to Th2 cytokine, IL-4, was halted in s100a4-deleted TAMs, as well as in bone marrow-derived macrophages, and as well as in Raw264.7 cells. Further molecular analyses reveal that CD36, downstream from S100A4-PPARγ, is the major effector for lipid uptake of S100A4+ macrophages. FurthermoreImportantly, higher levels of S100A4 is closely associated with tumor resistance to chemotherapy in murine models as well as poor prognosis of cancer patients in clinic . Our study thus suggests that blocking S100A4 constitutes a treatment strategy to reprogram macrophages toward an antitumor state by inhibiting PPAR-γ-induction mediated gene up-regulation.
2021-06-30 | GSE161060 | GEO
Project description:Whole lens transcriptome profiling by RNA-seq analysis was performed to investigate the role of S100A4 in lens architecture and function. These studies yielded the intriguing discovery that absence of S100A4 in the lens results in robust induction of gene expression of S100A5, an olfactory sensory neuron specific protein, and of genes encoding various photoreceptor and Müller glial cell proteins
2020-01-19 | GSE143909 | GEO
Project description:The identification of molecular characteristics that define metastatic disease is a primary research focus across numerous types of malignancies. Understanding the mechanisms that drive metastatic foci, which diverge significantly from the biology of primary tumors, and identifying new biomarkers specifically associated with metastatic disease, is of critical importance in oncology. Consequently, the characterization of the stroma associated with metastatic foci has been largely unexplored and remains an area requiring significant investigation. We identified a detailed transcriptional profile of the stromal compartment within primary tumors and corresponding metastatic foci using spatially resolved approaches. The identified stromal Met signature may serve as a prognostic biomarker and provide insights into the molecular mechanisms underlying the metastatic potential of the tumor microenvironment.
2024-08-04 | GSE273439 | GEO