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Fibroblast-specific reduction of heparan sulfate suppresses colon tumor growth and pancreatic cancer growth in mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Mus

PROVIDER: GSE203602 | GEO | 2022/06/13

REPOSITORIES: GEO

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Fibroblast-specific reduction of heparan sulfate suppresses colon tumor growth in mice

Project description:we examined how HS-reduced fibroblasts are involved in the proliferation of colon cancer by using mice in which Ext-1 expression is specifically suppressed in fibroblasts.

2022-06-13 | GSE203597 | GEO

Fibroblast-specific reduction of heparan sulfate suppresses pancreatic cancer growth in mice

Project description:we examined how HS-reduced fibroblasts are involved in the proliferation of pancreatic cancer by using mice in which Ext-1 expression is specifically suppressed in fibroblasts.

2022-06-13 | GSE203598 | GEO

Fibroblast-specific reduction of heparan sulfate suppresses colon tumor growth in mice

Project description:Fibroblast-specific reduction of heparan sulfate suppresses colon tumor growth in mice

| PRJNA841566 | ENA

Fibroblast-specific reduction of heparan sulfate suppresses colon tumor growth and pancreatic cancer growth in mice

Project description:Fibroblast-specific reduction of heparan sulfate suppresses colon tumor growth and pancreatic cancer growth in mice

| PRJNA841572 | ENA

Fibroblast-specific reduction of heparan sulfate suppresses pancreatic cancer growth in mice

Project description:Fibroblast-specific reduction of heparan sulfate suppresses pancreatic cancer growth in mice

| PRJNA841564 | ENA

Endothelial cell-specific reduction of heparan sulfate suppresses glioma growth in mice

Project description:we examined how HS-reduced vascular endothelial cells are involved in the proliferation of glioma by using mice in which Ext-1 expression is specifically suppressed in vascular endothelial cells.

2021-11-17 | GSE175419 | GEO

Endothelial cell-specific reduction of heparan sulfate suppresses glioma growth in mice.

Project description:PurposeHeparan sulfate (HS) is one of the factors that has been suggested to be associated with angiogenesis and invasion of glioblastoma (GBM), an aggressive and fast-growing brain tumor. However, it remains unclear how HS of endothelial cells is involved in angiogenesis in glioblastoma and its prognosis. Thus, we investigated the effect of endothelial cell HS on GBM development.MethodsWe generated endothelial cell-specific knockout of Ext1, a gene encoding a glycosyltransferase and essential for HS synthesis, and murine GL261 glioblastoma cells were orthotopically transplanted. Two weeks after transplantation, we examined the tumor progression and underlying mechanisms.ResultsThe endothelial cell-specific Ext1 knockout (Ext1 CKO ) mice exhibited reduced HS expression specifically in the vascular endothelium of the brain capillaries compared with the control wild-type (WT) mice. GBM growth was significantly suppressed in Ext1 CKO mice compared with that in WT mice. After GBM transplantation, the survival rate was significantly higher in Ext1 CKO mice than in WT mice. We investigated how the effect of fibroblast growth factor 2 (FGF2), which is known as an angiogenesis-promoting factor, differs between Ext1 CKO and WT mice by using an in vivo Matrigel assay and demonstrated that endothelial cell-specific HS reduction attenuated the effect of FGF2 on angiogenesis.ConclusionsHS reduction in the vascular endothelium of the brain suppressed GBM growth and neovascularization in mice.Supplementary informationThe online version contains supplementary material available at 10.1007/s12672-021-00444-3.

| S-EPMC8585801 | biostudies-literature

Endothelial cell-specific reduction of heparan sulfate suppresses glioma growth in mice

Project description:Endothelial cell-specific reduction of heparan sulfate suppresses glioma growth in mice

| PRJNA732371 | ENA

Heparan Sulfate Domains Required for Fibroblast Growth Factor 1 and 2 Signaling through Fibroblast Growth Factor Receptor 1c.

Project description:A small library of well defined heparan sulfate (HS) polysaccharides was chemoenzymatically synthesized and used for a detailed structure-activity study of fibroblast growth factor (FGF) 1 and FGF2 signaling through FGF receptor (FGFR) 1c. The HS polysaccharide tested contained both undersulfated (NA) domains and highly sulfated (NS) domains as well as very well defined non-reducing termini. This study examines differences in the HS selectivity of the positive canyons of the FGF12-FGFR1c2 and FGF22-FGFR1c2 HS binding sites of the symmetric FGF2-FGFR2-HS2 signal transduction complex. The results suggest that FGF12-FGFR1c2 binding site prefers a longer NS domain at the non-reducing terminus than FGF22-FGFR1c2 In addition, FGF22-FGFR1c2 can tolerate an HS chain having an N-acetylglucosamine residue at its non-reducing end. These results clearly demonstrate the different specificity of FGF12-FGFR1c2 and FGF22-FGFR1c2 for well defined HS structures and suggest that it is now possible to chemoenzymatically synthesize precise HS polysaccharides that can selectively mediate growth factor signaling. These HS polysaccharides might be useful in both understanding and controlling the growth, proliferation, and differentiation of cells in stem cell therapies, wound healing, and the treatment of cancer.

| S-EPMC5313116 | biostudies-literature

Compositional analysis of heparin/heparan sulfate interacting with fibroblast growth factor.fibroblast growth factor receptor complexes.

Project description:Heparan sulfate (HS) proteoglycans (PGs) interact with a number of extracellular signaling proteins, thereby playing an essential role in the regulation of many physiological processes. One major function of HS is to interact with fibroblast growth factors (FGFs) and their receptors (FGFRs) and form FGF.HS.FGFR signaling complexes. Past studies primarily examined the selectivity of HS for FGF or FGFR. In this report, we used a new strategy to study the structural specificity of HS binding to 10 different FGF.FGFR complexes. Oligosaccharide libraries prepared from heparin, 6-desulfated heparin, and HS were used for the interaction studies by solution competition surface plasmon resonance (SPR) and filter trapping assays. Specific oligosaccharides binding to FGF.FGFR complexes were subjected to polyacrylamide gel electrophoresis (PAGE) analysis and disaccharide compositional analysis using liquid chromatography and mass spectrometry. The competition SPR studies using sized oligosaccharide mixtures showed that binding of each of the tested FGFs or FGF.FGFR complexes to heparin immobilized to an SPR chip was size-dependent. The 6-desulfated heparin oligosaccharides exhibited a reduced level of inhibition of FGF and FGF.FGFR complex binding to heparin in the competition experiments. Heparin and the 6-desulfated heparin exhibited higher levels of inhibition of the FGF.FGFR complex binding to heparin than of FGF binding to heparin. In the filter trapping experiments, PAGE analysis showed different affinities between the FGF.FGFR complexes and oligosaccharides. Disaccharide analysis showed that HS disaccharides with a degree of polymerization of 10 (dp10) had high binding selectivity, while dp10 heparin and dp10 6-desulfated heparin showed reduced or no selectivity for the different FGF.FGFR complexes tested.

| S-EPMC3348549 | biostudies-literature

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