Differential regulation of glial cell line-derived neurotrophic factor (GDNF) expression in human neuroblastoma and glioblastoma cell lines

1999 ◽  
Vol 55 (2) ◽  
pp. 187-197 ◽  
Author(s):  
A.N. Verity ◽  
T.L. Wyatt ◽  
W. Lee ◽  
B. Hajos ◽  
P.A. Baecker ◽  
...  
Keyword(s):  
Cell Line ◽  
Glial Cell ◽  
Cell Lines ◽  
Neurotrophic Factor ◽  
Differential Regulation ◽  
Glioblastoma Cell ◽  
Human Neuroblastoma ◽  
Glioblastoma Cell Lines

Increase in secretion of glial cell line-derived neurotrophic factor from glial cell lines by inhibitors of vacuolar ATPase

2003 ◽  
Vol 42 (6) ◽  
pp. 493-498 ◽  
Author(s):  
Mariko Nishiguchi ◽  
Kimiko Tokugawa ◽  
Kyoko Yamamoto ◽  
Tomoko Akama ◽  
Yuriko Nozawa ◽  
...  
Keyword(s):  
Cell Line ◽  
Glial Cell ◽  
Cell Lines ◽  
Neurotrophic Factor ◽  
Vacuolar Atpase

scholarly journals The lipid phosphatase activity of PTEN is critical for stabilizing intercellular junctions and reverting invasiveness

2001 ◽  
Vol 155 (7) ◽  
pp. 1129-1136 ◽  
Author(s):  
Larissa Kotelevets ◽  
Jolanda van Hengel ◽  
Erik Bruyneel ◽  
Marc Mareel ◽  
Frans van Roy ◽  
...  
Keyword(s):  
Cell Line ◽  
Phosphatase Activity ◽  
Cell Lines ◽  
Dependent Manner ◽  
Glioblastoma Cell ◽  
Wild Type ◽  
Invasive Phenotype ◽  
Lipid Phosphatase ◽  
Glioblastoma Cell Lines ◽  
E Cadherin

To analyze the implication of PTEN in the control of tumor cell invasiveness, the canine kidney epithelial cell lines MDCKras-f and MDCKts-src, expressing activated Ras and a temperature-sensitive v-Src tyrosine kinase, respectively, were transfected with PTEN expression vectors. Likewise, the human PTEN-defective glioblastoma cell lines U87MG and U373MG, the melanoma cell line FM-45, and the prostate carcinoma cell line PC-3 were transfected. We demonstrate that ectopic expression of wild-type PTEN in MDCKts-src cells, but not expression of PTEN mutants deficient in either the lipid or both the lipid and protein phosphatase activities, reverted the morphological transformation, induced cell–cell aggregation, and suppressed the invasive phenotype in an E-cadherin–dependent manner. In contrast, overexpression of wild-type PTEN did not counteract Ras-induced invasiveness of MDCKras-f cells expressing low levels of E-cadherin. PTEN effects were not associated with marked changes in accumulation or phosphorylation levels of E-cadherin and associated catenins. Wild-type, but not mutant, PTEN also reverted the invasive phenotype of U87MG, U373MG, PC-3, and FM-45 cells. Interestingly, PTEN effects were mimicked by N-cadherin–neutralizing antibody in the glioblastoma cell lines. Our data confirm the differential activities of E- and N-cadherin on invasiveness and suggest that the lipid phosphatase activity of PTEN exerts a critical role in stabilizing junctional complexes and restraining invasiveness.

Heterogeneity and modulation of tumor-associated antigens in human glioblastoma cell lines

1989 ◽  
Vol 71 (3) ◽  
pp. 388-397 ◽  
Author(s):  
Marco Colombatti ◽  
Bruno Dipasquale ◽  
Lorena Del-l'Arciprete ◽  
Massimo Gerosa ◽  
Giuseppe Tridente
Keyword(s):  
Cell Surface ◽  
Cell Line ◽  
Cell Lines ◽  
Glioblastoma Cell ◽  
Heterogeneous Distribution ◽  
Human Glioblastoma ◽  
Human Glioblastoma Cell ◽  
Tumor Associated Antigens ◽  
Glioblastoma Cell Lines

✓ Seven human glioblastoma cell lines established in vitro from primary tumor explants were studied. A marked heterogeneity of glial fibrillary acidic protein was observed whereas vimentin was uniformly expressed by all cell lines. Indirect immunofluorescence and flow cytofluorometry revealed a heterogeneous distribution of surface GE 2 and CG 12 tumor-associated antigens (TAA's): three cell lines were positive (> 69% TAA-positive cells) and three cell lines were negative (< 9% TAA-positive cells). One cell line (Hu 228) was moderately positive at early culture passages and subsequently acquired a TAA-negative phenotype. The difference in the relative amounts of surface TAA's of the three positive cell lines was less than twofold. In spite of the heterogeneous distribution of surface TAA's, all cell lines exhibited considerable amounts of intracellular TAA. Treatment with phorbol esters and density-dependent growth arrest decreased the percentage of the TAA-positive cells and the amount of cell-surface TAA's in one cell line (Hu 195). Interferon-γ treatment in vitro increased the percentage of CG 12-positive cells by 12% and the amount of cell-surface CG 12 antigens by 38% as compared to untreated cells. The percentage of TAA-positive cells among phorbol ester-treated cells of the Hu 195 cell line was lowest 48 hours after treatment, but returned to normal values within the next 48 hours. Reduction of 3H-thymidine incorporation preceded the decrease in number of TAA-positive cells by about 18 hours. Two-color fluorescence analysis performed in positive cell lines for simultaneous determination of surface TAA's and deoxyribonucleic acid content or reactivity with the proliferation-associated Ki67 intracellular marker indicated that GE 2 and CG 12 antigens are expressed preferentially by actively proliferating glioma cells. The results of this study indicate the existence of two different phenotypes in cultured human glioblastoma cells: surface TAA-positive/cytosol TAA-positive and surface TAA-negative/cytosol TAA-positive cell populations. In addition, modulation of TAA expression was dependent on the cell-cycle differentiation stage, culture conditions, and proliferative state of the cells.

P13.09 Inconsistent effect of temozolomide exposure on cell viability in glioblastoma cell line models - a systematic review

2021 ◽  
Vol 23 (Supplement_2) ◽  
pp. ii34-ii34
Author(s):  
M M C Bruce ◽  
M T C Poon ◽  
P M Brennan
Keyword(s):  
Systematic Review ◽  
Cell Viability ◽  
Cell Line ◽  
Cell Lines ◽  
Exposure Duration ◽  
Laboratory Research ◽  
Glioblastoma Cell Line ◽  
Glioblastoma Cell ◽  
Glioblastoma Cell Lines ◽  
Common Cell

Abstract BACKGROUND The alkylating agent temozolomide is part of standard care for patients with glioblastoma. Potential novel therapeutic agents are often first evaluated against temozolomide in glioblastoma cell line models. Despite the importance of this step in compound development, there is no standard concentration or exposure duration of temozolomide in laboratory research, and consistency in the effect of temozolomide on glioblastoma cell lines has not been assessed. This systematic review aimed to summarise the concentration and exposure duration of temozolomide and its effect on cell viability in studies using glioblastoma cell lines. MATERIAL AND METHODS We searched Medline and Embase Jan 1994 - Feb 2021 for studies that used at least one glioblastoma cell line and reported a measure of cell viability associated with temozolomide exposure. Studies were excluded if they used modified cell lines or did not report a cell viability measure associated with temozolomide as monotherapy. One reviewer screened all records and two reviewers assessed potentially eligible studies for inclusion. The main data items included the cell lines used, the concentration and exposure duration to temozolomide, and cell viability measures. We summarised findings using descriptive statistics. RESULTS Of 1,533 potentially eligible studies we included 213 studies reporting 209 different cell lines. The most common cell lines were U87, U251 and T98G, used in 61%, 41%, and 27% of studies, respectively. Twenty-five (12%) studies used patient-derived cell lines. The concentration of temozolomide used ranged from 0 to 8000μM. The temozolomide exposure duration ranged from &lt;24 hours to &gt;96 hours, with 29% studies using 72 hours. The most common cell viability measure was half maximal inhibitory concentration (IC50), which was reported in 183 (86%) studies. The median IC50 in 32 studies using the U87 cell line was 180μM (interquartile range [IQR]: 52–254μM) at 48-hour temozolomide exposure and 202μM (IQR 52–518μM) at 72-hour exposure. The median IC50 in 31 studies using U251 cell line was 84μM (IQR: 34–324μM) at 48-hour exposure and 102μM (IQR: 35–358μM) at 72-hour exposure. CONCLUSION Experimental setup of temozolomide and its effect on cell viability vary widely between studies using similar glioblastoma cell lines. This inconsistency of response to temozolomide questions reproducibility and the translational value of study findings.

DDRE-16. DRUG REPURPOSING SCREEN REVEALS GLIOBLASTOMA CELL LINE SUSCEPTIBILITY TO STATINS

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi77-vi78
Author(s):  
Dylan Harwood ◽  
Signe Michaelsen ◽  
Filip Mundt ◽  
Bjarne Kristensen
Keyword(s):  
Cell Viability ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gene Knockout ◽  
Tumor Resection ◽  
Glioblastoma Cell ◽  
Potential Drug ◽  
Drug Candidates ◽  
Glioblastoma Cell Lines

Abstract BACKGROUND The standard therapy for glioblastoma patients is tumor resection followed by radiotherapy and temozolomide chemotherapy. Although glioblastoma has been extensively molecularly profiled along with other cancers, this knowledge has not yet been translated into improved survival outcomes. We used a bioinformatics approach to identify potential novel therapeutic strategies for glioblastoma. OBJECTIVES: Comprehensive online datasets which have assessed up to 1376 cancer cell lines in multiple ways were interrogated to identify potential drug candidates for glioblastoma. METHODS Datasets included were from the cancer cell line encyclopedia (mRNA expression), the Achilles project (cell viability following Crispr-Cas9 knockout) and PRISM (drug treatment). A t-test comparing cell viability of glioblastoma cell lines versus other cancers was used to identify potential drug candidates, followed by the use of multiple statistical tools to investigate potential mechanism of action and status of biomarkers. RESULTS Fluvastatin and pitavastatin produced the most significant effects in glioblastoma cell lines. The anti-cancer properties of statins have previously been attributed to the inhibition of HMG-Coa reductase. Here, we found their effects correlated with erastin, an enhancer of ferroptosis and with gene knockout of UBIAD1, which participates in non-mitochondrial ubiquinone synthesis. These effects were both found in glioblastoma cells and other cancers with a mesenchymal-like phenotype. CONCLUSION Statins appeared to be especially effective against glioblastoma lines and the effect could be linked to ferroptosis and inhibition of UBIAD1. In vitro validation of this finding is ongoing.

scholarly journals Propranolol Inhibits the Proliferation of Human Glioblastoma Cell Lines Through Notch1 and Hes1 Signaling System

2021 ◽  
Author(s):  
Hyun Sik Kim ◽  
Young Han Park ◽  
Mi Jung Kwon ◽  
Joon Ho Song ◽  
In Bok Chang
Keyword(s):  
Cell Proliferation ◽  
Cell Line ◽  
Cell Lines ◽  
Mtt Assay ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line ◽  
Glioblastoma Cell ◽  
Rt Pcr ◽  
Human Glioblastoma ◽  
Glioblastoma Cell Lines

Abstract PurposeThe anti-tumor effect of the beta-adrenergic receptor antagonist propranolol in breast cancer is well known; however, its activity in glioblastoma is not well-evaluated. The Notch-Hes pathway is known to regulate cell differentiation, proliferation, and apoptosis. We investigated the effect of propranolol to human glioblastoma cell lines, and the role of Notch and Hes signaling in this process.MethodsWe performed immunohistochemical staining on 31 surgically resected primary human glioblastoma tissues. We also used glioblastoma cell lines of U87-MG, LN229, and neuroblastoma cell line of SH-SY5Y in this study. The effect of propranolol and isoproterenol on cell proliferation was evaluated using the MTT assay (absorbance 570nm). The impact of propranolol on gene expression (Notch and Hes) was evaluated using real-time (RT) PCR, whereas protein levels of Notch1 and Hes1 were measured using western blotting (WB), simultaneously. Small interfering RNA (siRNA) was used to suppress the Notch gene to investigate its role in the proliferation of glioblastoma.ResultsPropranolol and isoproterenol caused a dose-dependent decrease in cell proliferation (MTT assay). RT-PCR showed an increase in Notch1 and Hes1 expression by propranolol, whereas WB demonstrated increase in Notch1 protein, but a decrease in Hes1 by propranolol. The proliferation of U87-MG and LN229 was not significantly suppressed after transfection with Notch siRNA.ConclusionThese results demonstrated that propranolol suppressed the proliferation of glioblastoma cell lines and neuroblastoma cell line, and Hes1 was more closely involved than Notch1 was in glioblastoma proliferation.

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