scholarly journals The HDAC6/8/10 inhibitor TH34 induces DNA damage-mediated cell death in human high-grade neuroblastoma cell lines

2018 ◽  
Vol 92 (8) ◽  
pp. 2649-2664 ◽  
Author(s):  
Fiona R. Kolbinger ◽  
Emily Koeneke ◽  
Johannes Ridinger ◽  
Tino Heimburg ◽  
Michael Müller ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
High Grade ◽  
Neuroblastoma Cell Lines

scholarly journals The Role of MYCN in the Failure of MYCN Amplified Neuroblastoma Cell Lines to G1 Arrest After DNA Damage

Cell Cycle ◽  
2006 ◽  
Vol 5 (22) ◽  
pp. 2639-2647 ◽  
Author(s):  
Emma Bell ◽  
Rakesh Premkumar ◽  
Jane Carr ◽  
Xiaohong Lu ◽  
Penny E Lovat ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
G1 Arrest ◽  
Neuroblastoma Cell Lines

No evidence of DNA damage by co-exposure to extremely low frequency magnetic fields and aluminum on neuroblastoma cell lines

2017 ◽  
Vol 823 ◽  
pp. 11-21 ◽  
Author(s):  
Milena Villarini ◽  
Angela Gambelunghe ◽  
Daniela Giustarini ◽  
Maria Vittoria Ambrosini ◽  
Cristina Fatigoni ◽  
...  
Keyword(s):  
Dna Damage ◽  
Magnetic Fields ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
Low Frequency ◽  
Extremely Low Frequency ◽  
Neuroblastoma Cell Lines

Abstract 3553: Cepharanthine reverses multidrug resistance sensitizing neuroblastoma cell lines to vincristine-induced cell death

2010 ◽  
Author(s):  
Regina M. Graham ◽  
James D. Guest ◽  
John W. Thompson ◽  
Keith A. Webster ◽  
Steven Vanni
Keyword(s):  
Cell Death ◽  
Multidrug Resistance ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Lines

In Vitro Evaluation of Apoptosis and Cell Death of Neuroblastoma Cell Lines Exposed to Busulfan.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4459-4459
Author(s):  
Morris Kletzel ◽  
Sarah C. Tallman ◽  
Marie Olszewski ◽  
Wei Huang
Keyword(s):  
Cell Death ◽  
Cell Viability ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
Annexin V ◽  
Resistant Cell ◽  
Primary Tumors ◽  
Induced Apoptosis ◽  
Neuroblastoma Cell Lines

Abstract Objective: While busulfan is a commonly used chemotherapeutic agent in the treatment of many hematological diseases, its effectiveness against neuroblastoma is still in question. This study aims to assess the degree of apoptosis and cell death in neuroblastoma cell lines and primary neuroblastoma tumors when exposed to varying doses of busulfan. Materials and Methods: Cultures from established cell lines SKN-SH, SKN-DOX-R, IMR-5, and NGP (n=4), as well as cultures from primary tumors (n=2) were seeded at 106 cells/ml in RPMI640 supplemented with 10% fetal bovine serum (FBS) and transferred to 24-well plates, where cells were exposed to 1ml of busulfan at 0, 0.001, 0.005, 0.01, 0.05, and 0.1mg/ml per well. Cells were incubated at 37°C in a humidified atmosphere of 5% CO2 for 72 hours. Wells were sacrificed after 0, 6, 24, 48 and 72 hours and tested with Annexin V and PI; 10,000 events were measured by flow cytometry. The percentage of apoptotic and dead cells was plotted in a graph and a t-test was performed against the untreated control. Results: After 24 hours, there was a significant decrease in cell viability of each dose when compared to the control untreated cells (p<0.005). 24 Hour % Cell Viability for Varying Doses of Busulfan (mg/ml) Dose 0 Dose 0.001 Dose 0.005 Dose 0.01 Dose 0.05 Dose 0.1 Mean 66.1 44.4 40.3 40.7 37.7 39 SEM 5.56 5.17 5.96 6.17 6.03 5.60 Median 65 33.5 38 39 37 31 Range 39 to 97 14 to 87 4 to 89 6 to 93 4 to 77 5 to 88 The overall mean decrease in cell viability when compared to the control was 25.7%. However, there were only modest differences in effectiveness when comparing the doses, with an average of only 5–7% difference between doses. Further, there was much variability between the different cell lines, some with changes in apoptosis and cell death of over 50%, while other lines showed no changes at all. Limited differences were seen after 6 hours, and after 72 hours any effect of busulfan was masked by cell death due to other factors, as seen through increased cell death in untreated cells. Conclusion: Busulfan induced apoptosis and cell death in vitro in neuroblastoma cell lines at a mean of 76.43% for non-resistant lines, 59.33% for primary tumors and 35% for resistant cell lines (at middle dose 0.01mg/ml). The resistance of certain cell lines confirms the difficulties of treating multi-drug resistant cells in often heterogeneous neuroblastoma tumors. That some cell lines were responsive shows the potential of using busulfan to treat neuroblastoma in the future.

Flow cytometry analysis of single-strand DNA damage in neuroblastoma cell lines using the F7-26 monoclonal antibody

2007 ◽  
Vol 71A (11) ◽  
pp. 951-960 ◽  
Author(s):  
Rita S. Grigoryan ◽  
Bo Yang ◽  
Nino Keshelava ◽  
Jerry R. Barnhart ◽  
C. Patrick Reynolds
Keyword(s):  
Monoclonal Antibody ◽  
Flow Cytometry ◽  
Dna Damage ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
Single Strand ◽  
Flow Cytometry Analysis ◽  
Neuroblastoma Cell Lines

scholarly journals MIAT Is an Upstream Regulator of NMYC and the Disruption of the MIAT/NMYC Axis Induces Cell Death in NMYC Amplified Neuroblastoma Cell Lines

2021 ◽  
Vol 22 (7) ◽  
pp. 3393
Author(s):  
Barbara Feriancikova ◽  
Tereza Feglarova ◽  
Lenka Krskova ◽  
Tomas Eckschlager ◽  
Ales Vicha ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Neuroblastoma Cell ◽  
Potential Therapeutic Target ◽  
Tissue Samples ◽  
Upstream Regulator ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Neuroblastoma Cell Lines ◽  
Transcriptional Target

Neuroblastoma (NBL) is the most common extracranial childhood malignant tumor and represents a major cause of cancer-related deaths in infants. NMYC amplification or overexpression is associated with the malignant behavior of NBL tumors. In the present study, we revealed an association between long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) and NMYC amplification in NBL cell lines and MIAT expression in NBL tissue samples. MIAT silencing induces cell death only in cells with NMYC amplification, but in NBL cells without NMYC amplification it decreases only the proliferation. MIAT downregulation markedly reduces the NMYC expression in NMYC-amplified NBL cell lines and c-Myc expression in NMYC non-amplified NBL cell lines, but the ectopic overexpression or downregulation of NMYC did not affect the expression of MIAT. Moreover, MIAT downregulation results in decreased ornithine decarboxylase 1 (ODC1), a known transcriptional target of MYC oncogenes, and decreases the glycolytic metabolism and respiratory function. These results indicate that MIAT is an upstream regulator of NMYC and that MIAT/NMYC axis disruption induces cell death in NMYC-amplified NBL cell lines. These findings reveal a novel mechanism for the regulation of NMYC in NBL, suggesting that MIAT might be a potential therapeutic target, especially for those with NMYC amplification.

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