Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA281656 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comparison of parental GSC (GSC-parental) with treatment resistant GSC clones survived 500uM TMZ treatment (GSC-500uM TMZ) We used microarrays to identify defense profiles of GSC-500uM TMZ
2015-10-01 | GSE68029 | GEO
Project description:Comparison of treatment sensitive GSC clones (TSGC) with treatment resistant GSC clones (TRGC). We used microarrays to identify molecular signatures of TRGC (upregulated genes). We used radiation treatment (RT) or RT plus TMZ to select treatment resistant GSC clones (TRGC)
2013-11-01 | E-GEOD-46531 | biostudies-arrayexpress
Project description:Acquired resistance of temozolomide (TMZ) is one of the major obstacle of glioblastoma clinical treatment and the mechanism of TMZ resistance is still not very clear. In the presented research we show that deletion of rs16906252-associated MGMT enhancer in MGMT negative glioma cells induced increase sensitivity to temozolomide and combination of RNA-seq and Capture HiC identified several long-range target genes of rs16906252-associated MGMT enhancer. In addition, HiC data shows alterations of chromatin structures in glioma cells survived from high-dosage TMZ treatment and changes of TADs influence rs16906252-associated MGMT enhancer’s long-range regulations of target genes. Our study suggests rs16906252-associated MGMT enhancer regulates glioma cells’ TMZ sensitivity by long-range regulations of several target genes, which is a novel mechanism of regulation of TMZ sensitivity in glioma cells.
2020-04-02 | GSE129476 | GEO
Project description:Expression data from glioblastoma stem cell clones (GSC)
| PRJNA200791 | ENA
Project description:<p>Glioblastoma multiforme (GBM) is highly aggressive, with treatment resistance and recurrence driven by metabolically plastic glioma stem cells (GSCs). Inspired by brown adipose tissue (BAT) thermogenesis, researchers transplanted BAT-derived mitochondria (BA-Mito) into GSCs, reducing stemness markers and enhancing chemosensitivity to temozolomide (TMZ). To improve delivery, a CD133 aptamer-modified liposome-coated mitochondrial system (Apt/Lipo-Mito Gel) was developed, using alginate hydrogel as a post-surgical reservoir for sustained mitochondrial release, offering a novel metabolic therapy strategy for GBM.</p>
2025-08-27 | MTBLS12901 | MetaboLights
Project description:Glioblastoma (GBM) is among the most aggressive cancers. Despite aggressive radiotherapy and treatment with the alkylating agent temozolomide (TMZ), patients ultimately succumb to the disease. Although much interest has focused on highly tumorigenic GBM stem cells (GSCs), adaption of a concept from microbial research proposes that a minor population of dormant âpersisterâ cells in cancer evade current therapies. To separate dormant and treatment-resistant tumor cells in human GBM tumorspheres, we have refined density gradient protocols previously used for separation of neurosphere-forming neural stem cells (NSCs). We find that a minor cell population in human GBM tumorsphere cultures and patient-derived tumor biopsies display increased cell density. These high-density GBM cells (HDGCs) display dormancy, variable expression of proposed GSC markers, and 10-100 fold higher levels of reprogramming gene expression compared to low-density GBM cells (LDGCs). Transcriptional profiling data confirmed the slow-cycling state of HDGCs. As a result, HDGCs show decreased tumorsphere formation capacity in vitro and reduced tumorigenicity in vivo. Using tumorspheres and xenografts, we demonstrated that HDGCs show increased treatment-resistance to ionizing radiation (IR) and temozolomide treatment compared to LDGCs. Similar to the NSC lineage, our data suggest that dormant HDGCs become increasingly sensitive to anti-proliferative therapies as they become activated and further differentiate. In conclusion, density gradients represents a marker-independent approach to separate dormant and treatment-resistant tumor cells in human GBMs and other solid cancers. 12 samples, no replicates, derived from 5 individual patients
2016-07-01 | E-GEOD-71116 | biostudies-arrayexpress
Project description:Glioblastoma stem cell (GSC) cultures are initiated from glioblastoma (GBM) surgical resection tissue. They can capture and propagate key GBM primary tumor molecular and cellular features. We have deeply characterized four IDH-expressing (IDH+ or ‘wildtype’) GSC cultures from unrelated adults to serve as cellular models for the majority of adult primary GBM. We demonstrate that GSC cultures can be continuously propagated in defined, serum-free media and 5% oxygen without requiring specialized growth substrates; have well-defined genomic and mtDNA variants and gene/protein expression profiles; and highly reproducible dose-survival curves when treated with the GBM standard-of-care therapies of ionizing radiation (IR) and temozolomide (TMZ). We also illustrate how expressed lentiviral barcodes, mtDNA variants and single cell gene expression profiling can be used to define and track cellular heterogeneity over 40 days after IR treatment. These well-characterized IDH+ GSC cultures can support many high throughput in vitro assay formats, including xenograft, organoid and other GBM disease modeling protocols. They should prove a useful resource to better understand GBM biology, and to identify new and more effective GBM therapies and treatment regimens.
2026-01-28 | GSE303662 | GEO
Project description:Background. Glioblastoma multiforme (GBM) exhibits a cellular hierarchy with a subpopulation of stem-like cells known as glioblastoma stem cells (GSCs), that drive tumor growth and contribute to treatment resistance. NAD(H) emerged as a crucial factor influencing GSCs. Methods. A multistep process of machine learning algorithms was implemented to construct the glioma stemness-related score (GScore). Further in silico and patient tissue analyses validated the predictive ability of the GScore and identified a potential target, CYP3A5. Loss-of-function or gain-of-function genetic experiments were performed to assess the impact of CYP3A5 on the self-renewal and chemoresistance of GSCs both in vitro and in vivo. Mechanistic studies were conducted using nontargeted metabolomics, RNA-seq, seahorse, transmission electron microscopy, immunofluorescence, flow cytometry, ChIP‒qPCR, RT‒qPCR, western blotting, etc. The efficacy of pharmacological inhibitors of CYP3A5 was assessed in vivo. Results. Based on the proposed GScore, we identify a GSC target CYP3A5, which is highly expressed in GSCs and temozolomide (TMZ)-resistant GBM patients. This elevated expression of CYP3A5 is attributed to transcription factor STAT3 activated by EGFR signaling or TMZ treatment. Depletion of CYP3A5 impairs self-renewal and TMZ resistance in GSCs. Mechanistically, CYP3A5 maintains mitochondrial fitness to promote GSC metabolic adaption through the NAD⁺/NADH-SIRT1-PGC1α axis. Additionally, CYP3A5 enhances the activity of NAD-dependent enzyme PARP to augment DNA damage repair. Treatment with CYP3A5 inhibitor alone or together with TMZ effectively suppresses tumor growth in vivo. Conclusion. Together, this study suggests that GSCs activate STAT3 to upregulate CYP3A5 to fine-tune NAD⁺/NADH for the enhancement of mitochondrial functions and DNA damage repair, thereby fueling tumor proliferation and conferring TMZ resistance, respectively. Thus, CYP3A5 represents a promising target for GBM treatment.
2025-01-08 | GSE277539 | GEO
Project description:Glioblastoma stem cell cultures (GSCs) are initiated from glioblastoma (GBM) surgical resection tissue, and can capture and propagate key GBM molecular and cellular features. We have deeply characterized four IDH-wildtype GSCs from unrelated adults as cellular models of a majority of adult primary GBMs. These GSC cultures could be continuously propagated in defined, serum-free media and 5% oxygen without requiring specialized growth substrates. They had well-defined genomic and mtDNA variants and gene and protein expression profiles. All four had highly reproducible dose response curves to the GBM standard-of-care therapies of ionizing radiation (IR) and temozolomide (TMZ). Expressed lentiviral barcodes, mtDNA variants and single cell gene expression profiling were used to define cellular heterogeneity, and to track individual cell trajectories and their gene expression programs over 40 days after IR treatment. These well-characterized GSC cultures can support many high throughput in vitro assay formats, as well as xenograft, organoid and other GBM disease modeling approaches. Their use should help to better understand GBM biology, and to identify new and more effective GBM therapies and treatment regimens.
2026-01-28 | GSE302554 | GEO
Project description:Glioblastoma stem cell cultures (GSCs) are initiated from glioblastoma (GBM) surgical resection tissue, and can capture and propagate key GBM molecular and cellular features. We have deeply characterized four IDH-wildtype GSCs from unrelated adults as cellular models of a majority of adult primary GBMs. These GSC cultures could be continuously propagated in defined, serum-free media and 5% oxygen without requiring specialized growth substrates. They had well-defined genomic and mtDNA variants and gene and protein expression profiles. All four had highly reproducible dose response curves to the GBM standard-of-care therapies of ionizing radiation (IR) and temozolomide (TMZ). Expressed lentiviral barcodes, mtDNA variants and single cell gene expression profiling were used to define cellular heterogeneity, and to track individual cell trajectories and their gene expression programs over 40 days after IR treatment. These well-characterized GSC cultures can support many high throughput in vitro assay formats, as well as xenograft, organoid and other GBM disease modeling approaches. Their use should help to better understand GBM biology, and to identify new and more effective GBM therapies and treatment regimens.
2026-01-28 | GSE303069 | GEO