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Effect of extracellular S100A4 on melanoma cells of different phenotypes

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE65897 | GEO | 2015/02/13

SECONDARY ACCESSION(S): PRJNA275330

REPOSITORIES: GEO

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Effect of extracellular S100A4 on melanoma cells of different phenotypes

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

Effect of knockdown of S100A4 on gene expression in A549 cells

Project description:S100A4 is a tumor metastasis-promoting protein and drives lung cancer cell invasion and its elevation level is associated with lymphovascular invasion and the decreased overall survival among lung cancer patients. However, how it alters cancer cell metabolism and how metabolic changes affect the invasive and metastatc capacity are unknown.

2019-03-15 | GSE121628 | GEO

RNA sequencing of porcine smooth muscle cells, after treatments with platelet derived growth factor and S100A4 protein

Project description:Smooth muscle cells were treated with platelet derived growth factor (PDGF-BB) and S100A4 protein to decipher the mechanisms by which they contribute to smooth muscle cell phenotypic transition. We report that PDGF-BB treatment upregulates genes related to growth response or to extracellular matrix component proteases, while S100A4 upregulates pro-inflammatory genes. When used in combination, PDGF-BB and S100A4 show synergistic action by enhancing the upregulation of genes already affected by S100A4 and by inducing the upregulation of genes exclusive for this condition.

2022-01-20 | GSE143296 | GEO

S100A4+ Stromal Cells from Normal Lung vs. Metastatic Lung

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

Macrophagic S100A4 drives macrophage protumor activation and promotes tumor growth through controlling PPAR-γ induction

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

Dysfunction of S100A4+ effector memory CD8+ T cells aggravates asthma

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

Comparison of gene expression profiles between S100A4-positive and -negative cells isolated from the Peyer's patches

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

Differential gene expression profile of S100A4 null mouse lens

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

S100A4+ Stromal Cells from Normal Lung vs. Metastatic Lung

Project description:Analysis of S100A4+ stromal cells at the gene expression level in physiological setting versus metastatic setting.

2011-08-30 | GSE31711 | GEO

The lipid droplet protein DHRS3 is a regulator of melanoma cell state

Project description:Lipid droplets are fat storage organelles composed of a protein envelope and a lipid rich core. Dynamic regulation of this protein envelope underlies differential lipid droplet formation and function in diverse cell types. In melanoma, the ability to form lipid droplets has been linked to tumor progression and metastasis, but it is not known whether lipid droplet proteins play a role in these phenotypes. To address this, we performed proteomic analysis of the lipid droplet envelope in melanoma. We found that proteins expressed in the lipid droplet were differentially enriched in distinct melanoma states, ranging from melanocytic to neural crest like. DHRS3, which is involved in the conversion of all-trans-retinal to all-trans-retinol, is significantly upregulated in the MITFLO/neural crest-like melanoma cell state, and markedly reduced in the MITFHI/melanocytic state. Increased DHRS3 expression is sufficient to drive the MITFHI/melanocytic cells to a more undifferentiated and invasive state. These changes are due to retinoic acid mediated regulation of melanocytic genes through the retinoid X receptors (RXR). Our data demonstrate that melanoma cell state can be regulated by expression of lipid droplet proteins which affect downstream retinoid signaling.

2024-03-25 | GSE262095 | GEO

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