Inhibition of cell invasion by indomethacin on glioma cell lines: in vitro study

2005 ◽  
Vol 72 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Maode Wang ◽  
Daizo Yoshida ◽  
Shouxun Liu ◽  
Akira Teramoto
2009 ◽  
Vol 28 (5) ◽  
pp. 554-560 ◽  
Author(s):  
Efstathia Giannopoulou ◽  
Konstantinos Dimitropoulos ◽  
Andreas A. Argyriou ◽  
Angelos K. Koutras ◽  
Fotinos Dimitrakopoulos ◽  
...  

2017 ◽  
Vol 32 (9) ◽  
pp. 344-350
Author(s):  
Elena Vasilskis ◽  
Ingrid Kreimerman ◽  
Silvia Olivera ◽  
Eduardo Savio ◽  
Henry Engler

2008 ◽  
Vol 586 (1-3) ◽  
pp. 24-34 ◽  
Author(s):  
Andressa Bernardi ◽  
Rudimar L. Frozza ◽  
Eliézer Jäger ◽  
Fabrício Figueiró ◽  
Luci Bavaresco ◽  
...  

2019 ◽  
Vol 7 (4) ◽  
pp. 91-96
Author(s):  
Isra'a Al-sobhi ◽  
◽  
Rawan Al-Ghabban ◽  
Soad Shaker Ali ◽  
Jehan Al-Amri ◽  
...  

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Michael T. C. Poon ◽  
Morgan Bruce ◽  
Joanne E. Simpson ◽  
Cathal J. Hannan ◽  
Paul M. Brennan

Abstract Background Malignant glioma cell line models are integral to pre-clinical testing of novel potential therapies. Accurate prediction of likely efficacy in the clinic requires that these models are reliable and consistent. We assessed this by examining the reporting of experimental conditions and sensitivity to temozolomide in glioma cells lines. Methods We searched Medline and Embase (Jan 1994-Jan 2021) for studies evaluating the effect of temozolomide monotherapy on cell viability of at least one malignant glioma cell line. Key data items included type of cell lines, temozolomide exposure duration in hours (hr), and cell viability measure (IC50). Results We included 212 studies from 2789 non-duplicate records that reported 248 distinct cell lines. The commonest cell line was U87 (60.4%). Only 10.4% studies used a patient-derived cell line. The proportion of studies not reporting each experimental condition ranged from 8.0–27.4%, including base medium (8.0%), serum supplementation (9.9%) and number of replicates (27.4%). In studies reporting IC50, the median value for U87 at 24 h, 48 h and 72 h was 123.9 μM (IQR 75.3–277.7 μM), 223.1 μM (IQR 92.0–590.1 μM) and 230.0 μM (IQR 34.1–650.0 μM), respectively. The median IC50 at 72 h for patient-derived cell lines was 220 μM (IQR 81.1–800.0 μM). Conclusion Temozolomide sensitivity reported in comparable studies was not consistent between or within malignant glioma cell lines. Drug discovery science performed on these models cannot reliably inform clinical translation. A consensus model of reporting can maximise reproducibility and consistency among in vitro studies.


2020 ◽  
Vol 47 (8) ◽  
pp. 3691-3702 ◽  
Author(s):  
Elisabeth Mara ◽  
Monika Clausen ◽  
Suphalak Khachonkham ◽  
Simon Deycmar ◽  
Clara Pessy ◽  
...  

2020 ◽  
Vol 38 (1) ◽  
pp. 36-46
Author(s):  
Jnanranjan Panda ◽  
Bhabani Sankar Satapathy ◽  
Bidisha Mandal ◽  
Ramkrishna Sen ◽  
Biswajit Mukherjee ◽  
...  

2015 ◽  
Vol 16 (12) ◽  
pp. 9936-9948 ◽  
Author(s):  
Mustafa El-Khatib ◽  
Carolin Tepe ◽  
Brigitte Senger ◽  
Maxine Dibué-Adjei ◽  
Markus Riemenschneider ◽  
...  

2019 ◽  
Vol 18 ◽  
pp. 153303381882140 ◽  
Author(s):  
Ye Zhang ◽  
Rui Zhang ◽  
Rui Sui ◽  
Yi Chen ◽  
Haiyang Liang ◽  
...  

MicroRNA-374a has been abnormally expressed in several cancer types; however, its role in glioma remains unclear. Therefore, we aimed to investigate whether microR-374a participated in the progression of glioma. Expression of microR-374a in glioma cell lines and normal cell line was measured by quantitative real-time polymerase chain reaction. Luciferase reporter assay and Western blot were used to detect the targets of microR-374a. In vitro functional experiments were conducted to investigate the biological role of microR-374a. Low expression of microR-374a was found in glioma cell lines. Prokineticin 2 was identified as a direct target of microR-374a in glioma. Investigations on the mechanisms related to glioma progression showed that microR-374a inhibited glioma cell proliferation, cell cycle progression, and cell invasion through targeting Prokineticin 2. Taken together, these results revealed that microR-374a functions as tumor suppressor by targeting Prokineticin 2, suggesting it might be a novel therapeutic target for glioma.


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