scholarly journals MicroRNA-374a Governs Aggressive Cell Behaviors of Glioma by Targeting Prokineticin 2

2019 ◽  
Vol 18 ◽  
pp. 153303381882140 ◽  
Author(s):  
Ye Zhang ◽  
Rui Zhang ◽  
Rui Sui ◽  
Yi Chen ◽  
Haiyang Liang ◽  
...  
Keyword(s):  
Cell Lines ◽  
Glioma Cell ◽  
Cell Cycle Progression ◽  
Luciferase Reporter ◽  
Cell Behaviors ◽  
Prokineticin 2 ◽  
Glioma Cell Lines ◽  
Glioma Cell Proliferation ◽  
Cancer Types

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.

scholarly journals lncRNA LINC00355 Acts as a Novel Biomarker and Promotes Glioma Biological Activities via the Regulation of miR-1225/FNDC3B

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Zhen-yong Qi ◽  
Li-li Wang ◽  
Xu-liang Qu
Keyword(s):  
Cell Lines ◽  
Glioma Cell ◽  
Biological Activities ◽  
Glioma Cells ◽  
Disease Free Survival ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Glioma Cell Lines

Background. Accumulating evidence has implicated long noncoding RNAs (lncRNAs) in glioma progression. Here, we aimed to explore the potential roles of a novel lncRNA, LINC00355, in glioma and to clarify the underlying mechanisms. Methods. RT-PCR was used to examine the relative expressions of LINC00355 in glioma cell lines and specimen samples. The clinicopathological and prognostic significances of LINC00355 in glioma patients were statistically analyzed. To determine cell activities, CCK-8, clonogenic assays, flow cytometry, migration, and invasion assays were performed. Moreover, the potential mechanisms of LINC00355 were investigated by bioinformatics assays and luciferase reporter assays. Results. LINC00355 expression was increased in glioma cell lines and specimens, and higher LINC00355 expression predicted advanced clinical progress and reduced overall survival and disease-free survival in glioma patients. Functionally, LINC00355 depletion promoted cell proliferation, invasion, and migration in glioma cells and induced apoptosis of glioma cells, whereas LINC00355 upregulation resulted in the opposite effects in vitro. Mechanistic assays revealed that LINC00355 as a sponge for miR-1225 repressed fibronectin type III domain-containing 3B (FNDC3B) expressions. Conclusion. Our findings revealed the tumor-promotive roles of LINC00355 in the progression of glioma, indicating that LINC00355 exhibited ceRNA functions via modulating miR-1225/FNDC3B axis.

scholarly journals Temozolomide sensitivity of malignant glioma cell lines – a systematic review assessing consistencies between in vitro studies

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Michael T. C. Poon ◽  
Morgan Bruce ◽  
Joanne E. Simpson ◽  
Cathal J. Hannan ◽  
Paul M. Brennan
Keyword(s):  
Cell Viability ◽  
Malignant Glioma ◽  
Cell Line ◽  
Cell Lines ◽  
Glioma Cell ◽  
Glioma Cell Line ◽  
In Vitro Studies ◽  
Experimental Conditions ◽  
Glioma Cell Lines

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.

scholarly journals Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell Proliferation and Invasion by Interacting with MiR-16

2018 ◽  
Vol 46 (3) ◽  
pp. 1055-1064 ◽  
Author(s):  
Xin Chen ◽  
Deheng Li ◽  
Yang Gao ◽  
Wei Tang ◽  
Lao IW ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Glioma Cell ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Glioma Cell Lines ◽  
Glioma Cell Proliferation ◽  
Proliferation And Invasion

Background/Aims: Long noncoding RNAs (lncRNAs) are a novel class of protein-noncoding transcripts that are aberrantly expressed in multiple diseases including cancers. LINC00152 has been identified as an oncogene involved in many kinds of cancer; however, its expression pattern and function in human glioma remain unclear. Methods: Quantitative real-time polymerase chain reaction was carried out to measure LINC00152 expression in human glioma cell lines and tissues. CCK-8 and EdU assays were performed to assess cell proliferation, and scratch assays and Transwell assays were used to assess cell migration and invasion, respectively. Luciferase reporter assays were carried out to determine the interaction between miR-16 and LINC00152. In vivo experiments were conducted to assess tumor formation. Results: LINC00152 was found to be significantly upregulated in human glioma cell lines and clinical samples. Knockdown of LINC00152 suppressed glioma cell proliferation, migration, and invasion in vitro. In vivo assays in nude mice confirmed that LINC00152 knockdown inhibits tumor growth. Furthermore, mechanistic investigation showed that LINC00152 binds to miR-16 in a sequence-specific manner and suppresses its expression. miR-16 inhibition strongly attenuated LINC00152 knockdown–mediated suppressive effects on proliferation, migration, and invasion. Moreover, LINC00152 induced BMI1 expression by sponging miR-16; this effect further promoted glioma cell proliferation and invasion. Conclusion: We regard LINC00152 as an oncogenic lncRNA promoting glioma cell proliferation and invasion and as a potential target for human glioma treatment.

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
Keyword(s):  
Cell Lines ◽  
Cell Invasion ◽  
Glioma Cell ◽  
In Vitro Study ◽  
Vitro Study ◽  
Glioma Cell Lines

In vitro uptake of a new cholesteryl carborane ester compound by human glioma cell lines

2004 ◽  
Vol 93 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Gina Peacock ◽  
Richard Sidwell ◽  
Guangliang Pan ◽  
Svein Øie ◽  
D.Robert Lu
Keyword(s):  
Cell Lines ◽  
Glioma Cell ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Glioma Cell Lines ◽  
In Vitro Uptake

scholarly journals An in vitro study, evaluating the effect of sunitinib and/or lapatinib on two glioma cell lines

2009 ◽  
Vol 28 (5) ◽  
pp. 554-560 ◽  
Author(s):  
Efstathia Giannopoulou ◽  
Konstantinos Dimitropoulos ◽  
Andreas A. Argyriou ◽  
Angelos K. Koutras ◽  
Fotinos Dimitrakopoulos ◽  
...  
Keyword(s):  
Cell Lines ◽  
Glioma Cell ◽  
In Vitro Study ◽  
Vitro Study ◽  
Glioma Cell Lines

scholarly journals ET-9 Development of photosensitive antibodies for near-infrared light immunotherapy targeting EGFR and IL13Rα2 of malignant gliomas and investigation of their photodynamic cytotoxic activity in vitro

2021 ◽  
Vol 3 (Supplement_6) ◽  
pp. vi5-vi5
Author(s):  
Naosuke Nonoguchi ◽  
Akihiro Kambara ◽  
Seigo Kimura ◽  
Shinji Kawabata ◽  
Ryokichi Yagi ◽  
...  
Keyword(s):  
Cytotoxic Activity ◽  
Cell Lines ◽  
Glioma Cell ◽  
Near Infrared ◽  
Malignant Gliomas ◽  
Cellular Heterogeneity ◽  
Phase Iii ◽  
Infrared Light ◽  
Glioma Cell Lines

Abstract Introduction: Near-Infrared Photoimmunotherapy (NIR-PIT) is a recently developed hybrid cancer therapy based on photodynamic cytotoxicity and anti-tumor immunopotentiation, utilizing a photosensitive antibody drug (PSAD). A global Phase III trial of NIR-PIT with an anti-EGFR-PSAD in patients with recurrent head and neck squamous cell carcinoma (HNSCC) is already underway, and NIR-PIT is expected to have therapeutic applications also in malignant gliomas. Methods: In this study, monoclonal antibodies to EGFR and IL13Rα2 were conjugated to the photosensitive dye IRDye700DX (IR700) to produce PSADs (EGFR-Ab/IR700 and IL13Rα2-Ab/IR700) and in vitro PDT assays using these PSADs were performed on four human glioma cell lines (U87MG, U251, U138, A172).Five groups were studied: EGFR-Ab/IR700 monotherapy: 5 μg/ml or 10 μg/ml, IL13Rα2-Ab/IR700 monotherapy: 5 μg/ml or 10 μg/ml, and EGFR-Ab/IR700: 5 μg/ml + IL13Rα2-Ab/IR700: 5 μg/ml combination therapy. The cytotoxic activity of each group was compared after irradiation with 690 nm light at 16 J/cm2. Results: Significantly higher cytotoxic activity was observed in all four glioma cell lines when EGFR-Ab/IR700 and IL13Rα2-Ab/IR700 were used in combination at 5 μg/ml each, than when each PSAD was treated with a doubled dose (10 μg/ml).Conclusion: Malignant gliomas show extensive cellular heterogeneity with diverse expression of cell surface antigens. The present results suggest that a therapeutic strategy using several different photosensitive antibodies simultaneously may lead to the release of tumor antigens from a greater number of tumor cells, resulting in a more efficient host immune response for therapeutic purposes.

scholarly journals CBMT-31. HDAC INHIBITION DIMINISHES THE GROWTH OF ENDOGENOUS IDH MUTANT GLIOMAS

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi39-vi40
Author(s):  
Lubayna Elahi ◽  
Matthew Garrett ◽  
Lea Guo ◽  
Michael Condro ◽  
Riki Kawaguchi ◽  
...  
Keyword(s):  
Cell Lines ◽  
Transcriptional Repression ◽  
Glioma Cell ◽  
Histone Deacetylase Inhibitors ◽  
Sequencing Analysis ◽  
Hdac Inhibition ◽  
In Vivo Experiments ◽  
Glioma Cell Lines

Abstract Histone deacetylase inhibitors (HDACi’s) have emerged as a promising class of drugs for treatment of malignancies such as glioblastoma (GBM). Several studies have demonstrated the anti-tumor property of HDACi’s against GBM in both in vitro and in vivo experiments. Nonetheless, in clinical trials, HDACi only marginally increased overall survival of patients with GBM. The mixed results of trials with HDACi’s in glioma have prompted us to hypothesize that improved selection of patients by tumor characteristics could enhance the efficacy of therapy. We specifically tested the effects of valproic acid (VPA), a HDACi and an antiepileptic drug against IDH mutant gliomas. We have previously demonstrated that our IDH mutant glioma cell lines have gene expression and methylation patterns highly similar to IDH mutant tumors in situ. Mutant IDH1 alters the epigenetic landscape of gliomas leading to the hypermethylation phenotype and transcriptional repression of genes. This repression of genes may contribute to tumorigenesis and progression of IDH mutant gliomas. We found that VPA inhibits the growth of patient-derived IDH1 mutant glioma lines. In addition, RNA sequencing analysis of vehicle and VPA-treated IDH1 mutant glioma cells showed de-repression of several genes previously shown to be downregulated in IDH1 mutant glioma cell lines. We also treated cells with another HDACi LBH589 and found that both VPA and LBH589 upregulates similar gene sets suggesting that HDAC inhibition promotes de-repression of previously repressed genes. Ongoing studies are aimed at determining the molecular mechanism by which VPA regulates the growth of IDH1 mutant tumors.

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