Differential gene expression analysis between adherent U87MG cells and U87MG cell-derived glioma stem-like cells (P4E8 cells).
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE146698 | GEO | 2021/06/10
REPOSITORIES: GEO
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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:Differential gene expression analysis between adherent U87MG cells and U87MG cell-derived glioma stem-like cells (P4E8 cells).
| PRJNA611698 | ENA
Project description:EGFRvA is a novel and widely-expressed EGFR isoform, whose upregulation is positively related to glioma grades. Intriguingly, it is the upregulation of EGFRvA but not EGFR that significantly correlates with a poor prognosis in glioma patients. Cancer cells expressing EGFRvA (relative to EGFR) display a higher invasive capacity and a lower sensitivity to EGFR tyrosine kinase inhibitors (TKIs). To investigate the significant differently expressed genes between U87MG EGFRvA cells and U87MG EGFR cells，microarray experiments were conducted.
2012-09-30 | GSE41230 | GEO
Project description:EGFRvA is a novel and widely-expressed EGFR isoform, whose upregulation is positively related to glioma grades. Intriguingly, it is the upregulation of EGFRvA but not EGFR that significantly correlates with a poor prognosis in glioma patients. Cancer cells expressing EGFRvA (relative to EGFR) display a higher invasive capacity and a lower sensitivity to EGFR tyrosine kinase inhibitors (TKIs). To investigate the significant differently expressed genes between U87MG EGFRvA cells and U87MG EGFR cellsM-oM-<M-^Lmicroarray experiments were conducted. Gene-expression profiling was performed on the CapitalBio 35k human Genome Array microchips (Beijing, China).
2012-09-30 | E-GEOD-41230 | biostudies-arrayexpress
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 “persister” 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.
2016-07-01 | GSE71116 | GEO
Project description:This study investigated the biological function of CD133 by ectopic expression of CD133 in U87MG cell line. Although CD133 is widely used as a cancer stem cell marker, there are a few studies that examined its own biological functions. While a number of loss-of-function studies about CD133 have shown that CD133 have effects on cancer progression, there are few gain-of-function studies about functions of CD133. Thus, we identified the potential function of CD133 by its overexpression in U87MG glioblastoma cell line. Though there were no significant changes in cell growth and sphere forming ability, elevated IL-1β and its downstream chemokines (CCL3, CXCL3, CXCL5) may function as chemoattractants which affect recruitment of Ly6G+ neutrophils surrounding necrotic regions in vivo and migration of neutrophil-like dHL-60 cells. Taken together, this results imply that CD133 can regulate IL-1β signaling, and promotes the environmental change.
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Project description:Differential transcriptome analysis between control cells (U87MG), TMZ-resistant cells with continuous TMZ treatment (U87MG R50) and TMZ-resistant cells with interrupted treatment (U87MG OFF R50).
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Project description:The recent identification of cancer stem cells (CSCs) in multiple human cancers provides a new inroad to understanding tumorigenesis at the cellular level. CSCs are defined by their characteristics of self-renewal, multipotentiality, and tumor initiation upon transplantation. By testing for these defining characteristics, we provide evidence for the existence of CSCs in a transgenic mouse model of glioma, S100Ã-verbB;Trp53. In this glioma model, CSCs are enriched in the side-population (SP) cells. These SP cells have enhanced tumor-initiating capacity, self-renewal, and multipotentiality compared to non-SP cells from the same tumors. Furthermore, gene expression analysis comparing FACS-sorted cancer SP cells to non-SP cancer cells and normal neural SP cells identified 45 candidate genes that are differentially expressed in glioma stem cells. We validated the expression of two genes from this list (S100a4 and S100a6) in primary mouse gliomas and human glioma samples. Analyses of xenografted human GBM (glioblatoma multiforme) cell lines and primary human glioma tissues show that S100A4 and S100A6 are expressed in a small subset of cancer cells and that their abundance is positively correlated to tumor grade. In conclusion, this study shows that CSCs exist in a mouse glioma model, suggesting that this model can be used to study the molecular and cellular characteristics of CSCs in vivo and to further test the cancer stem cell hypothesis. Experiment Overall Design: This study features two factors, injected cell origin (either tumorsphere or neurosphere) and FACS cell population (either side population or non-side population cells). There were two different tumorspheres, labeled 3447 and 4346 that were isolated from brain tumors in S100beta-verbB;p53-/- or S100beta-verbB;p53+/- mice. The tumorspheres were injected separately into the brains of NOD.Cg-Prkdc<scid>Il2rg<tm1Wjl>/SzJ mice to generate biological triplicates of each primary tumor. Tumorspheres were isolated and cultured before FACS sorting to obtain side population and non-side population cells. As a control, untransformed neurospheres from three independent S100beta-verbB;p53-/- or S100beta-verbB;p53+/- mice were isolated, cultured, and FACS sorted to obtain side population and non-side population cells. Side population and non-side population cells cultured from three mice injected with the 3447 cultured tumorspheres were assayed for gene expression (six samples). Side-population stem cells cultured from three mice injected with the 4346 cultured tumorspheres were assayed for gene expression (three samples). Side-population and non-side population cells cultured from three mice injected with the neurospheres were assayed for gene expression (six samples).
2009-01-13 | E-GEOD-13490 | biostudies-arrayexpress
Project description:U87MG is a glioblastoma cell line that shows substantial heterogeneity despite long-term passaging. We used microarrays to identify variations in gene expression that are associated with phenotypic differences among subclones derived from U87MG.
2015-02-12 | GSE54967 | GEO
Project description:BACKGROUND: Triple-negative breast cancer (TNBC) is insensitive to the most effective therapies for other breast cancers, including endocrine and Her2-directed therapies, thus the lack of specific treatments prompted us to search for new TNBC-associated molecules to be used as targets for cancer therapy. As patients with TNBC usually experience a quicker relapse and metastatic progression compared to other breast cancer subtypes, we hypothesized that cancer stem cells (CSC) could play a central role in TNBC. We thus directed our focus on genes differentially expressed between CSC and differentiated cancer cells of TNBC cell lines. RESULTS: We established tumorsphere cultures from mouse and human mammary cancer cell lines to enrich the CSC population. RNA-Seq was used to identify differences in gene expression between tumorspheres and their monolayer counterparts. Seventy-four transcripts were found up-regulated in the tumorspheres, while forty-two genes were down-regulated. Enrichment analysis of biological processes showed an up-regulation in genes involved in regulation of apoptosis in tumorspheres, and a down-regulation in genes involved in lipid metabolism and cell cycle regulation. By focusing on up-regulated genes coding for cell membrane-associated proteins, we selected Teneurin-4 (TENM4) as a candidate for further studies. Meta-analysis of publicly available datasets revealed that TENM4 mRNA is up-regulated in both lobular and ductal invasive carcinoma specimens compared to normal breast, and that high expression of TENM4 in TNBC patients shows a trend of correlation with a shorter relapse-free survival. 4T1 tumorspheres treated with a siRNA specific to TENM4 showed a decrease in TENM4 mRNA and protein levels, which was reflected by a significant impairment of tumorsphere-forming ability. TENM4 silencing also led to a decrease in Focal Adhesion Kinase (FAK) phosphorylation, which has been previously linked to CSC biology, thus strengthening the possible link between TENM4 and a CSC-like phenotype. CONCLUSIONS: Overall, our results indicate that the stem-like status of TNBC cells is accompanied by altered regulation of apoptosis, cell cycle and lipid metabolism pathways. Furthermore, we identified TENM4 as a potential novel player in CSC biology, and its potential role as a novel target to improve the outcome of TNBC patients in the future.
2018-01-30 | GSE109798 | GEO