Expression data from mice brain implanted GSC272 glioma stem cells or POSTN knockout
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE73071 | GEO | 2015/09/16
SECONDARY ACCESSION(S): PRJNA295982
REPOSITORIES: GEO
Similar Datasets
Project description:Differential mRNA expression patterns were seen in GSC272-vector compared to GSC272-POSTN shRNA tumors. We used microarrays to POSTN regulated gene expression in glioma stem cells. Gene expression comparisons were shown between: 1. mRNA control from GSC272 glioma stem cells implanted mouse brain tumor at 7 weeks after implantation, and 2. mRNA deplection of POSTN from knock down of POSTN of GSC272 glioma stem cells implanted mouse brain tumor at 7 weeks after implantation.
2015-09-16 | E-GEOD-73071 | biostudies-arrayexpress
Project description:Bone fracture healing requires skeletal stem cells (SSCs), which facilitate intramembranous ossification and endochondral ossification in long bone fractures. Although the periosteum is necessary for bone homeostasis and regeneration, the in vivo origin and regulatory mechanisms of periosteal SSCs (P-SSCs) remain unclear. Here, we identified Postn+ P-SSCs at the cambium layer of the periosteum that actively orchestrate regeneration in response to bone injury. Notably, the Postn+ P-SSCs that arise during bicortical fractures are likely derived from Gli1+ P-SSCs. In addition, Postn+ cell ablation compromises cortical bone homeostasis and bone regeneration. The IGF signal is indispensable in the regulatory effect of Postn+ P-SSCs on bicortical fractures since the genetic deletion of Igf1r in Postn+ cells dampens bone fracture healing. Taken together, adult Postn+ cells are region-specific P-SSCs that contribute to bone homeostasis and regeneration and are partially dependent upon IGF signaling.
2024-10-16 | GSE255137 | GEO
Project description:Malignant gliomas are considered to be one of the deadliest human cancers, accounting for about 60% of all primary brain tumors. Cachexia is a complex metabolic derangement and muscle atrophy syndrome, which causes high mortalities in patients with advanced cancers including brain tumors. However, cachexia symptoms induced by gliomas and mechanisms underlying muscle atrophy are unclear. Herein, we developed a glioma cachexia model using nude mice orthotopicly implanted with two glioma cell lines (WHO II CHG5 and WHO IV U87). U87 mice developed more severe cachexia symptoms than CHG5 mice, including more evident anorexia, greater body weight loss and mortality. Unlike non-central nervous system cancer cachexia, glioma cachexia did not induce remarkable systemic inflammation but massive multi-organ atrophy. It also caused significantly decreased skeletal muscle mass and strength, which were associated with down-regulated myosin and AKT, and up-regulated AMPK, FOXO and Atrogin1. Interestingly, expressions of MuRF1, MyoD1, eIF3f, desmin and vimentin were not significantly changed. Consistently, NMR-based metabolomic analyses revealed pronounced metabolic derangements in cachectic gastrocnemius relative to controls. Glucose, glycerol, 3-hydroxybutyrate and glycine were remarkably down-regulated, whereas largely released amino acids due to proteolysis including glutamate, arginine, leucine and isoleucine were up-regulated in cachectic gastrocnemius. Moreover, glucose and lipid metabolism, protein biosynthesis and amino acid metabolism were disturbed dramatically in both glioma-bearing mice. U87 mice showed more changed metabolite levels and altered metabolic pathways. This work uncovers malignant grade-dependent glioma cachexia symptoms and metabolic derangements of skeletal muscle for the first time, and provides hints for new therapeutic approaches.
2018-09-22 | ST001064 | MetabolomicsWorkbench
Project description:This study is a part of series performed for the same researcher through pilot/feasibility grant program, so the publication is relevant reference for other studies (ST000199) This specific experiment is a pilot study to compare the metabolism of cells transformed using empty vector against cells transformed with vector carrying short hairpin RNA (shRNA) targeted to silence isocitrate dehydrogenase-1 (IDH1) gene.
2014-06-11 | ST000276 | MetabolomicsWorkbench
Project description:Incomplete thermal ablation may induce invasiveness of hepatocellur carcinoma, however, the mechasim is not fully understood. Here, we investigated whether activated hepatic stellate cells would accelerate the progression of residual HCC after sublethal heat treatment via the secretion of POSTN. We used microarrays to detail the global programme of up-regulated genes of residual HCC cells induced by POSTN.
2018-01-09 | GSE108853 | GEO
Project description:Glioblastoma (GBM), classified as a grade 4 glioma, is the most prevalent intrinsic malignancy of the central nervous system. Glioblastoma stem cells (GSCs) are small populations of GBM cells with self-renewal and multilineage differentiation capabilities and are considered responsible for the tumorigenesis and development of GBM. POSTN secreted from glioblastoma stem cells can recruit microglia and upregulate CD70 expression in microglia through the αVβ3/PI3K/AKT/NFκB pathway, which in turn promotes Treg development and functionality and supports the formation of an immunosuppressive tumor microenvironment.
2024-08-01 | GSE273251 | GEO
Project description:Analysis of the effects of targeting NOS2 at the gene expression level. Our studies demonstrated a role for NOS2 in glioma biology through the maintenance of the glioma stem cell phenotype. Microarray results provide novel targets of NOS2 and suggest mechanisms through which NOS2 contributes to glioma stem cell biology. Glioma stem cells isolated from two different human glioma xenografts were infected with a non-targeting control shRNA or two different shRNAs directed against NOS2 (each treatment in each tumor performed in technical duplicates).
2011-07-08 | E-GEOD-29750 | biostudies-arrayexpress
Project description:Tumor associated macrophages are contributing to local invasion, angiogensis, and metastasis during the progression of many kinds of tumor including glioma We used microrray to study the difference of expression of glioma associated macrophages and normal brain tissue associated macrophages The macrophgages were isolated based on the markers of GFP and F4/80+ from Gl261 glioma and normal brain, RNA were extracted for microarray analysis
2012-05-27 | E-GEOD-38283 | biostudies-arrayexpress
Project description:Acne keloidalis (AK) is a primary scarring alopecia characterized by longstanding inflammation in the scalp leading to keloid-like scar formation and hair loss. Histologically, AK is characterized by mixed leukocytic infiltrates in the acute stage followed by a granulomatous reaction and extensive fibrosis in later stages. To further explore its pathogenesis, bulk RNA-sequencing and single-cell RNA sequencing were applied to scalp biopsy specimens of lesional and adjacent non-lesional skin in patients with clinically active disease. Unbiased clustering revealed 18 distinct cell populations, including two notable populations, POSTN+ fibroblasts with enriched extracellular matrix signatures, and SPP1+ myeloid cells M2 macrophages. Cell communication analyses indicate that fibroblasts and myeloid cells communicate by collagen and SPP1 signaling networks in lesional skin. Tissue immunofluorescence staining demonstrated SPP1+ myeloid cells and POSTN+ fibroblasts at the upper segment of outer root sheath of the hair follicle in the subacute stage, confirming micro-anatomic specificity with relevant disease activity. Therapy with intralesional corticosteroids reduced SPP1 and POSTN expression, and lessened AK progression. In summary, the communication between POSTN+ fibroblasts and SPP1+ myeloid cells by collagen and SPP1 axis may contribute to the pathogenesis of AK.
2024-04-10 | GSE206790 | GEO
Project description:The goal of this study is to identify the mechanism for how ALK promotes tumorigenesis in neuroblastoma. We developed a human stem cell model of neuroblastoma and generated isogenic tumors using MYCN and MYCN/ALK. RNAseq analysis of both tumors revealed an enrichment in focal adhesion signaling and allowed us to find POSTN as a key mediator of ALK-mediated tumor growth.
2024-03-21 | GSE228194 | GEO