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Glycosyl-T expression in NB cells

ABSTRACT: Dr. Ladisch's work focuses on the establishment of the biological significance of gangliosides that are shed by tumor cells, particularly those involved in pediatric cancers, including brain tumors and neuroblastoma. These studies are directed toward illuminating the hypothesis that shed gangliosides enhance tumor formation, possibly both by inhibiting the antitumor immune response and by enhancing growth factor-induced signaling and proliferation of fibrobalsts and vascular endotheilial cells in the tumor microenvironment. Delineation of the signaling pathways affected by ganglioside exposure is currently under study.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE26481 | GEO | 2011/01/07

SECONDARY ACCESSION(S): PRJNA136505

REPOSITORIES: GEO

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Glycosyl-T expression in NB cells

Project description:Dr. Ladisch's work focuses on the establishment of the biological significance of gangliosides that are shed by tumor cells, particularly those involved in pediatric cancers, including brain tumors and neuroblastoma. These studies are directed toward illuminating the hypothesis that shed gangliosides enhance tumor formation, possibly both by inhibiting the antitumor immune response and by enhancing growth factor-induced signaling and proliferation of fibrobalsts and vascular endotheilial cells in the tumor microenvironment. Delineation of the signaling pathways affected by ganglioside exposure is currently under study. The effect of retinoic acid on the mRNA levels of ganglioside glycosyltransferases in neuroblastoma cells in vitro Experiment to determine mRNA expression for ganglioside glycosyltransferases in NB cells (untreated versus treated with ATRA) using the Glyco-gene Chip by the Consortium for Functional Glycomics. Human NB cell lines LAN-5 were incubated with 10 µM of all-trans retinoic acid or untreated as control, and total RNA harvested after 24 hours, 72 hours and 120 hours of exposure to retinoic acid. We performed three independent experiments on either cell line so that for each cell line and each time point three replicates were be obtained (total: 18 chips). Glycosyltransferases of particular interest are LacCer synthase, GlucCer synthase, GM3 synthase, GD3 synthase, GM2/GD2 synthase, GD1b/GM1a synthase, GT1b/GD1a synthase and GQ1b/GT1a synthase.

2011-01-07 | E-GEOD-26481 | biostudies-arrayexpress

Deficiency of the frontotemporal dementia gene GRN results in gangliosidosis

Project description:Haploinsufficiency of GRN causes frontotemporal dementia (FTD). The GRN locus produces progranulin (PGRN), which is cleaved to lysosomal granulin polypeptides. The function of lysosomal granulins and why their absence causes neurodegeneration are unclear. Here we discover that PGRN-deficient human cells and murine brains, as well as human frontal lobes from GRN-mutation FTD patients have increased levels of gangliosides, glycosphingolipids that contain sialic acid. In these cells and tissues, levels of lysosomal enzymes that catabolize gangliosides were normal, but levels of bis(monoacylglycero)phosphates (BMP), lipids required for ganglioside catabolism, were reduced with PGRN deficiency. Our findings indicate that granulins are required to maintain BMP levels to support ganglioside catabolism, and that PGRN deficiency in lysosomes leads to gangliosidosis. Lysosomal ganglioside accumulation may contribute to neuroinflammation and neurodegeneration susceptibility observed in FTD due to PGRN deficiency and other neurodegenerative diseases.

2022-09-18 | PXD035889 | Pride

Gene expression in natural killer cells specifically recruited to lymph nodes by tumors

Project description:Dr. Fukuda's laboratory focuses on the cellular and molecular biology of cell surface glycoproteins in development and cancer with a secial emphasis on immune and neural systems.

2011-04-29 | GSE28924 | GEO

Cell lines LS180 vs U937

2011-02-17 | GSE27351 | GEO

Genome-wide maps of histone H3K9/K14 acetylation state in HeLa cells control (Mock) or silenced for Gb3 globoside synthase (Gb3S_KD) or silenced for the epigenetic modulator AUTS2 (AUTS2_KD)

Project description:Glycosphingolipid metabolism is reprogrammed during neural development with a switch from globo to ganglio-series glycosphingolipids production. We discovered that globo-series glycosphingolipids repress the epigenetic regulator of neuronal genes expression AUTS2. AUTS2 in turn, binds and activates the promoter of the first and rate limiting ganglioside producing enzyme GM3 synthase, thus fostering the synthesis of gangliosides. By this mechanism the globo-AUTS2 axis controls glycosphingolipid reprogramming and neural genes expression during neural differentiation, which involves this circuit in neurodevelopment and its defects in neuropathology. We report Gb3 globoside suppresses the expression of the epigenetic modulator AUTS2. The silencing of Gb3 synthase in HeLa cells induces the thepletion of Gb3 globoside, consequentially promoting AUTS2 expression. AUTS2 in turn, binds and activates the promoter of the target genes promoting local histone hyperacetylation and gene expression. Thus, the globo-series glycosphingolipids, by counteracting the expression of AUTS2, decrease histone acetylation at neuronal gene promoters repressing their transcription in HeLa cells.

2017-12-22 | GSE107044 | GEO

Cell lines LS180 vs U937

Project description:Dr. Esko's laboratory focuses on the structure, function, and biosynthesis of glycoproteins and proteoglycans. This laboratory also works on the design and synthesis of small molecule inhibitors of glycosylation. We analyzed the expression patterns of glycosyltransferase, growth factors, and receptors in endothelial cells derived from NDST1 deficient and wild-type mice using cancer cell line types U937 and LS180 .

2011-02-17 | E-GEOD-27351 | biostudies-arrayexpress

SialidaseNeu3action on GM1 ganglioside is neuroprotective in GM1 Gangliosidosis

Project description:GM1 gangliosidosis is a neurodegenerative disorder caused by mutations in theGLB1gene, which encodes lysosomalb-galactosidase. The enzyme deficiency blocks GM1 ganglioside catabolism, leading to accumulation of GM1 ganglioside and asialo-GM1 ganglioside (GA1 glycolipid) in brain. This disease can present in varying degrees of severity, with the level of residualb-galactosidase activity primarily determining the clinical course.Glb1null mouse models, which completely lackb-galactosidase expression, exhibit a less severe form of the disease than expected from the comparable deficiency in humans, suggesting a potential species difference in the GM1 ganglioside degradation pathway. We hypothesized this difference may involve the sialidase NEU3, which acts on GM1 ganglioside to produce GA1 glycolipid. To test this hypothesis, we generatedGlb1/Neu3double knockout (DKO) mice. These mice had a significantly shorter lifespan, increased neurodegeneration, and more severe ataxia thanGlb1KO mice.Glb1/Neu3DKO mouse brains exhibited an increased GM1 ganglioside to GA1 glycolipid ratio compared withGlb1KO mice, indicating that Neu3 mediated GM1 ganglioside to GA1 glycolipid conversion inGlb1KO mice. The expression of genes associated with neuroinflammation and glial responses were enhanced inGlb1/Neu3DKO mice compared withGlb1KO mice. Mouse Neu3 more efficiently converted GM1 ganglioside to GA1 glycolipid than human NEU3 did. Our findings highlight Neu3’s role in ameliorating the consequences ofGlb1deletion in mice, provide insights into NEU3’s differential effects between mice and humans in GM1 gangliosidosis, and offer a potential therapeutic approach for reducing toxic GM1 ganglioside accumulation in GM1 gangliosidosis patients.

2023-12-14 | GSE241844 | GEO

Altered GM1 catabolism affects NMDAR-mediated Ca2+ signaling at ER-PM junctions and increases synaptic spine formation

Project description:GM1-ganglioside, an abundant GSL in neuronal membranes, is integral to ER-PM junctions where it interacts with synaptic proteins/receptors and regulates Ca2+ signaling.

2024-03-19 | PXD042994 | Pride

Gene expression analisys of GD2+ cells from metastatic NB, unselected bone marrow from metastatic NB, primary tumors from stage 4 NB (alive and dead at 5 years of follow-up) and primary tumor from localized NB

Project description:Metastases in the bone marrow (BM) are grim prognostic factors in patients with neuroblastoma (NB). In spite of extensive analysis of primary tumor cells from high- and low-risk NB patients, a characterization of freshly isolated BM-infiltrating metastatic NB cells is still lacking. Our aim was to identify proteins specifically expressed by metastatic NB cells, that may be relevant for prognostic and therapeutic purposes. Metastatic NB cells were freshly isolated from patients’ BM by positive immunomagnetic bead manipulation using anti-GD2 monoclonal antibody. Unselected BM samples from patients with metastatic NB were also included. Gene expression profiles were compared with those obtained from archived NB primary tumors from patients with 5y-follow-up. After validation by RT-qPCR, expression/secretion of the proteins encoded by the up-regulated genes in the BM-infiltrating NB cells was evaluated by flow cytometry and ELISA. Compared to primary tumor cells, BM-infiltrating NB cells down-modulated the expression of CX3CL1, AGT, ATP1A2 mRNAs, whereas they up-regulated several genes commonly expressed by various lineages of BM resident cells. BM-infiltrating NB cells expressed indeed the proteins encoded by the top-ranked genes, S100A8 and A9 (calprotectin), CD177 and CD3, and secreted the CXCL7 chemokine. BM-infiltrating NB cells also expressed CD271 and HLA-G. We have identified proteins specifically expressed by BM-infiltrating NB cells. Among them, calprotectin, a potent inflammatory protein, and HLA-G, endowed with tolerogenic properties facilitating tumor escape from host immune response, may represent novel biomarkers and/or targets for therapeutic intervention in high-risk NB patients.

2018-03-29 | GSE112447 | GEO

Silencing of the PHLDA1 leads to global proteome changes and differentiation pathways of human neuroblastoma cells

Project description:Neuroblastoma (NB) is the most common extracranial pediatric solid tumor originating from the abnormal development of cells of the sympathoadrenal lineage of the neural crest. Targeting GD2 ganglioside (GD2), a glycolipid expressed on neuroblastoma cells, with GD2 ganglioside-recognizing antibodies affects several pivotal signaling routes that drive or influence the malignant phenotype of the cells. Previously performed gene expression profiling helped us to identify the PHLDA1 (pleckstrin homology-like domain family A member 1) gene as the most upregulated gene in the IMR-32 human neuroblastoma cells treated with the mouse 14G2a monoclonal antibody. Mass spectrometry-based proteomic analyses were applied to better characterize a role of PHLDA1 protein in the response of neuroblastoma cells to chimeric ch14.18/CHO antibody. Additionally, global protein expression profile analysis in the IMR-32 cell line with PHLDA1 silencing revealed increase in biological functions of mitochondria, accompanied by differentiation-like phenotype of the cells. Moreover, mass spectrometry analysis of the proteins co-immunoprecipitated using anti-PHLDA1-specific antibody, selected a group of possible PHLDA1 binding partners. Also, a more detailed analysis suggested that PHLDA1 interacts with the DCAF7/AUTS2 complex, a key component of neuronal differentiation in vitro.

2024-02-15 | PXD044319 | Pride

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