RNA deep sequencing analysis of glioma stem cells(GSCs) and non-GSCs
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ABSTRACT:
PROVIDER: PRJNA423102 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6392170_1.fastq.gz | Fastqsanger.gz | |||
| SRR6392170_2.fastq.gz | Fastqsanger.gz | |||
| SRR6392171_1.fastq.gz | Fastqsanger.gz | |||
| SRR6392171_2.fastq.gz | Fastqsanger.gz | |||
| SRR6392172_1.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of Hoechst 33342 dye-effluxing side population cells (SP cells defined as glioma stem cells, GSCs) and dye-retaining main population cells (MP cells defined as non-GSCs) that were FACS-sorted from the C6 glioma cell line stably expressing EGFP (C6-eGFP). ECM-related genes, such as Col4a1 and Col4a2, and the iron carrier gene Tf are upregulated in MP cells. Results provide the insight into molecular basis underlying the maintenance of GSCs by non-GSCs. Gene expression profiles were compared between SP and MP cells just after FACS-sorting from the whole C6-eGFP cells based on their Hoechst-effluxing abilities.
2016-07-03 | E-GEOD-72431 | biostudies-arrayexpress
Project description:Analysis of Hoechst 33342 dye-effluxing side population cells (SP cells defined as glioma stem cells, GSCs) and dye-retaining main population cells (MP cells defined as non-GSCs) that were FACS-sorted from the C6 glioma cell line stably expressing EGFP (C6-eGFP). ECM-related genes, such as Col4a1 and Col4a2, and the iron carrier gene Tf are upregulated in MP cells. Results provide the insight into molecular basis underlying the maintenance of GSCs by non-GSCs.
2016-01-01 | GSE72431 | GEO
Project description:Glioma-derived stem-like cells (GSCs) are hypothesized to provide a repository of cells in tumors that can self-replicate and be resistant to radiation and chemotherapeutic agents developed for the treatment of tumors. The potential lack of response of GSCs to traditional cytotoxic and radiation therapies has significant implications for tumor biology and therapeutics. At M.D. Anderson Cancer Center, a large number of GSC lines representing several glioma sub-types have been isolated and characterized with respect to gene expression. In order to identify potential therapeutic targets relating to GSC phenotype, we examined protein expression in 35 GSC lines relative to an external protein standard using label-free quantitative proteomics. Samples were analyzed in triplicate by nanoLC-MS/MS (Orbitrap Elite, Thermo) in block-randomized groups of three GSCs plus the external standard. The resulting .raw files were aligned by group in Progenesis LC-MS (Nonlinear Dynamics). Database searching was performed with PEAKS 6 software (BSI) against a UniprotKB/SwissProt Human database appended with the cRAP contaminant database. Peptide intensities were exported for analysis in DanteR. The resulting relative fold changes were used to drive unsupervised hierarchical clustering of the cell lines for the purpose of classifying cell lines, and Ingenuity Pathway Analysis (IPA) and the DAVID webtool were used to determine the biochemical pathways and biological processes impacted by protein changes in each cell line. Within IPA, Upstream Analysis was used to predict biological functions and transcriptional regulators whose increased or decreased activity was consistent with the observed fold changes, and the resulting upstream regulators with significant z-scores were exported for unsupervised hierarchical clustering. In addition to showing upstream regulators known to be associated with glioma, including Myc, tumor protein 53 (TP53), N-myc proto-oncogene protein (MYCN), two novel upstream regulators, synoviolin 1 (SYVN1) and interleukin 5 (IL5) were identified. A cluster of proteins found to be decreased relative to mixed control in mesenchymal cell lines was subjected to further bioinformatics analysis, identifying SRSF2 as a potential upstream regulator.
2015-07-07 | PXD001890 | Pride
Project description:SUMMARY Terminal differentiation has been proposed as a therapeutic strategy for glioblastoma (GBM). Culturing of GBM derived tumor initiating glioma stem cells (GSCs) in fetal bovine serum containing media is a proposed mode of differentiation that is thought to induce loss of stem cell characteristics, promote neural lineage differentiation and a parallel loss of tumor initiation capacity. Here we show that GSCs retained both neurosphere formation and tumor initiation abilities after short or long term serum exposure. Under serum induced differentiating conditions, GSCs expressed both neural lineage and stem cell markers, highlighting the aberrant pseudo-differentiation state. GSCs maintained under adherent differentiating conditions continued to proliferate and initiate tumor formation with efficiencies similar to GSCs maintained under proliferating (neurosphere) conditions. Proneural (PN) GSCs under serum exposure showed an induction of mesenchymal (MES) gene expression signatures. Our data indicate that the tumor initiation ability of GSCs is independent of their differentiation state and that terminal differentiation as a therapeutic approach may not effectively negate tumorigenicity of GSCs. SIGNIFICANCE Terminal differentiation has been proposed as a therapeutic strategy for glioblastoma (GBM). Culturing of GBM derived tumor initiating glioma stem cells (GSCs) in fetal bovine serum containing media is a proposed mode of differentiation that is thought to induce loss of stem cell characteristics, promote neural lineage differentiation and a parallel loss of tumor initiation capacity. Here we show that GSCs retained both neurosphere formation and tumor initiation abilities after short or long term serum exposure. Under serum induced differentiating conditions, GSCs expressed both neural lineage and stem cell markers, highlighting the aberrant pseudo-differentiation state. GSCs maintained under adherent differentiating conditions continued to proliferate and initiate tumor formation with efficiencies similar to GSCs maintained under proliferating (neurosphere) conditions. Proneural (PN) GSCs under serum exposure showed an induction of mesenchymal (MES) gene expression signatures. Our data indicate that the tumor initiation ability of GSCs is independent of their differentiation state and that terminal differentiation as a therapeutic approach may not effectively negate tumorigenicity of GSCs.
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Project description:To explore potential molecular mechanisms underlying the temporal process of DNA damage and repair in CSCs, we utilized deep RNA sequencing to analyze the expression of DNA damage and repair-associated genes at the transcriptome level. Our gene set analysis of CSCs and matched non-CSCs revealed a stemness-associated upward trend of global gene expression, particularly in NHEJ, mismatch excision repair (MMR) and HR pathways.
2017-12-20 | GSE108322 | GEO
Project description:Tumor heterogeneity of high-grade glioma (HGG) is recognized by four clinically relevant subtypes based on core gene signatures. However, molecular signaling in glioma stem cells (GSCs) in individual HGG subtypes is poorly characterized. Here we identified and characterized two mutually exclusive GSC subtypes with distinct dysregulated signaling pathways. Analysis of mRNA profiles distinguished proneural (PN) from mesenchymal (Mes) GSCs and revealed a pronounced correlation with the corresponding PN or Mes HGGs. Mes GSCs displayed more aggressive phenotypes in vitro and as intracranial xenografts in mice. Further, Mes GSCs were markedly resistant to radiation compared with PN GSCs. The glycolytic pathway, comprising aldehyde dehydrogenase (ALDH) family genes and in particular ALDH1A3, were enriched in Mes GSCs. Glycolytic activity and ALDH activity were significantly elevated in Mes GSCs but not in PN GSCs. Expression of ALDH1A3 was also increased in clinical HGG compared with low-grade glioma or normal brain tissue. Moreover, inhibition of ALDH1A3 attenuated the growth of Mes but not PN GSCs. Last, radiation treatment of PN GSCs up-regulated Mes-associated markers and downregulated PN-associated markers, whereas inhibition of ALDH1A3 attenuated an irradiation-induced gain of Mes identity in PN GSCs. Taken together, our data suggest that two subtypes of GSCs, harboring distinct metabolic signaling pathways, represent intertumoral glioma heterogeneity and highlight previously unidentified roles of ALDH1A3-associated signaling that promotes aberrant proliferation of Mes HGGs and GSCs. Inhibition of ALDH1A3- mediated pathways therefore might provide a promising therapeutic approach for a subset of HGGs with the Mes signature.
2015-03-20 | GSE67089 | GEO
Project description:Abnormal activation of stemness factors is a crucial signature of cancer stem cells (CSCs), a highly tumorigenic subpopulation in malignant tumors. However, it is unclear whether multi-signaling pathways are activated in CSCs, as like normal stem cells. I would like to report that an inhibitor of differentiation 1 (ID1) activates intracellular multi-signaling involved in proliferation, genesis, and maintenance of glioma stem cells (GSCs) by suppression of Cullin3, an E3 ubiquitin ligase that degrades Cyclin E and components of SHH and WNT signaling. ID1 inhibits BMP-dependent differentiation of GSCs by activation of BMPR2-targeting miR17/20a. ID1HIGH-Cullin3LOW signature correlates with a poor prognosis of GBM patients with a significant association to gene signatures enriched in EGF, WNT, SHH, and BMP signaling. Combinational inhibition of GSC intracellular multi-signaling network increases tumor-bearing mice survival. These results provide insights on molecular and cellular basis of GSC biology, and also suggest necessity of multi-signaling inhibition for GSCs therapy. Two human primary glioma stem cells (GSCs) such as GSC2 and GSC8 were isolated from two individual primary human glioma specimens. The GSCs were directly transfected with pSuper-GFP-ID1-shRNA and pSuper-GFP-Scrambled-shRNA using FuGENE 6 reagent (Roche). The RNA extraction in these cells was used to analyze gene expression.
2013-09-05 | E-GEOD-40614 | biostudies-arrayexpress
Project description:he unique prolyl isomerase Pin1 that promotes protein conformational changes is a pivotal therapeutic target in many cancers, but little is known about the regulation of Pin1 protein stability. We previously found that Pin1 was highly expressed in glioma stem cells (GSCs) relative to non-stem tumor cells (NSTCs). Interestingly, treatment of the proteasome inhibitor MG132 markedly restored Pin1 protein expression in NSTCs to a level similar to GSCs. We therefore sought to identify the molecular regulators controlling the proteasomal degradation of Pin1 by mass spectrometry analysis of Pin1-interacting proteins in GSCs. The results showed that Pin1 interacts with a deubiquitinase USP34 in GSCs, suggesting that Pin1 may be stabilized by USP34.
2024-01-26 | PXD041043 | Pride
Project description:Glioblastoma is a malignant brain tumor that is highly resistant to radiation and chemotherapy, where patients survive on average only 15 months after diagnosis. Furthering the understanding of mechanisms leading to radiation resistance of glioma is paramount to identify novel therapeutic targets. Previous studies have shown that glioma stem cells (GSCs) play an important role in promoting radiation resistance and disease recurrence. Herein we analyze the proteomic alterations occurring in patient-derived GSCs upon radiation treatment in order to identify molecular drivers of resistance. We show that proteome changes upon radiation accurately predict the resistance status of the cells, and that resistance to radiation does not correlate with glioma transcriptional subtypes. We further show that the radio-resistant cell line GSC-267 sheds microvesicles (MVs) enriched in the metabolic enzyme nicotinamide phosphoribosyltransferase (NAMPT).
2023-04-06 | PXD030092 | Pride
Project description:Glioblastoma is the most malignant brain tumor in adults and is associated with poor survival despite multimodal treatments. Glioma stem cells (GSCs) are cells with properties reminiscent from the normal neural stem cells counterparts. They have been postulated to be the culprit of glioma chemo- and radio-resistance ultimately leading to relapse. Understanding the molecular circuits governing the GSC compartment is essential. Sox2, a critical transcription regulator of embryonic and neural stem cell function, is deregulated in GSCs, but the description of the precise molecular pathways regulated by this gene in GSCs remains poorly understood. Results: We performed a genome-wide analysis of Sox2-regulated transcripts in GSCs, using microarray. We identified a total of 135 differentially expressed coding transcripts and 261 non-coding transcripts (B value > 0). Cell adhesion and cell-cell signaling are among the most enriched terms using GO classification. The pathways altered after Sox2 down-modulation includes multiple cellular processes such as aminoacid metabolism and intercellular signaling cascades. We validate the top 5 down regulated coding genes and one of the top 5 up-regulated coding genes. We also defined and classify the set of non-coding transcripts differentially expressed regulated by Sox2 in GSCs, and validated two of them. Conclusions: We present a comprehensive analysis of the transcriptome controlled by Sox2 in GSCs, gaining insights in the understanding of the potential roles of Sox2 in glioblastoma.
2016-11-04 | GSE79302 | GEO