m6A RNA Methylation Controls Proliferation of Human Glioma Cells by Influencing Cell Apoptosis

2019 ◽  
Vol 159 (3) ◽  
pp. 119-125 ◽  
Author(s):  
Feng Li ◽  
Chao Zhang ◽  
Guifang Zhang
Keyword(s):  
Surgical Removal ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Glioma Tissue ◽  
Hsp90 Expression ◽  
Proliferation Ability ◽  
Aggressive Tumors ◽  
M6a Rna Methylation ◽  
High Level ◽  
U251 Cells

Glioma, as one of the most aggressive tumors, is hardly cleaned by surgical removal, leading to a low survival rate. m6A is an internal modification in RNA and plays an important role in many kinds of cancers. In our study, we detected that the m6A level was decreased in glioma tissue, which might be caused by decreased METTL3 and increased FTO levels. We upregulated the m6A level in U251 cells by overexpressing METTL3. The results showed that a high level of m6A led to a reduced migration and proliferation ability, and vice versa. Finally, we performed a TUNEL assay and showed that m6A regulated cell proliferation by influencing apoptosis of U251 cells through regulating HSP90 expression.

Baicalein Induces Autophagy and Apoptosis through AMPK Pathway in Human Glioma Cells

2019 ◽  
Vol 47 (06) ◽  
pp. 1405-1418 ◽  
Author(s):  
Bingyan Liu ◽  
Lingling Ding ◽  
Li Zhang ◽  
Shuang Wang ◽  
Yu Wang ◽  
...  
Keyword(s):  
Glioma Cell ◽  
Caspase 3 ◽  
Therapeutic Agents ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Dapi Staining ◽  
Ampk Pathway ◽  
Compound C ◽  
Anticancer Effects ◽  
U251 Cells

Baicalein (BAI) is a natural flavonoid. It has been shown that BAI has anticancer effects, but the molecular mechanism is still unclear. The aim of the current study was to confirm whether or not BAI triggers autophagy and induces AMPK activation in glioma U251 cells. The Ad-mcherry-GFP-LC3B adenovirus experiments indicated that BAI induces glioma cell autophagy. Western blotting showed that the level of LC3II expression increased with the time and concentration of BAI. Following treatment with chloroquine, the expression of LC3 was enhanced Immunofluorescence also confirmed this result. At the same time, cleaved caspase-3, DAPI staining, and JC-1 staining revealed that apoptosis was also induced in the induction of autophagy. In addition, we found that BAI activates phosphorylation of AMPK, which is further confirmed using compound C in this process. When the phosphorylation of AMPK was inhibited, autophagy, and apoptosis were also inhibited. In conclusion, BAI induces autophagy and apoptosis through AMPK pathway. Surprisingly, our research provides new insight with the function of anticancer of BAI, and the potential of the promotion in glioma cell apoptosis might be related to autophagy activation. These results demonstrate the anticancer activity of BAI, which can be used as potential therapeutic agents for cancer therapy.

Effects of Pokemon combined with survivin and cyclin B1 on glioma U251 cells by Fe3O4 magnetic nanoparticles

2019 ◽  
Vol 9 (6) ◽  
pp. 616-622
Author(s):  
Mo Wang ◽  
Shengqiang Jiang ◽  
Xu Zhang ◽  
Ruoyu Peng ◽  
Minghua Zhu ◽  
...  
Keyword(s):  
Cell Viability ◽  
Opposite Effect ◽  
Cyclin B1 ◽  
Tunel Staining ◽  
Potential Mechanism ◽  
Human Glioma ◽  
Fe3o4 Magnetic Nanoparticles ◽  
Glioma Tissue ◽  
Qrt Pcr ◽  
U251 Cells

Gliomas are the most common type of malignant brain tumors. Glioma diagnosis is not very effective, and there are few therapeutic biomarkers. The aims of this study were to detect Pokemon and its regulatory genes and explore the potential mechanism between them in glioma. The Fe3O4 nanoparticles identified using TEM were used to isolate cell and tissue RNA, qRT-PCR was used to detect Pokemon, survivin, and cyclin B1 mRNA expression. Western blotting was used to detect Pokemon, survivin, and cyclin B1 protein expression. Immunofluorescence and immunohistochemistry were used to detect Pokemon expression. CCK-8 assay, EdU staining, and TUNEL staining were used to assess cell viability and apoptosis. Pokémon was over-expressed in human glioma tissue and cells. In U251 cells, Pokemon knockdown significantly decreased survivin and cyclin B1 expression, cell viability, and Pokemon expression and increased apoptosis. Pokemon overexpression had an opposite effect. In addition, over-expressed Pokemon reversed these results. Overall, we found that Pokemon promotes tumorigenesis, and the potential mechanism might be related to the Pokemon-related genes survivin and cyclin B1.

Mutant IκBα Suppresses Hypoxia-Induced VEGF Expression Through Downregulation of HIF-1α and COX-2 in Human Glioma Cells

2005 ◽  
Vol 15 (3) ◽  
pp. 139-149 ◽  
Author(s):  
Yoshihira Kimba ◽  
Tatsuya Abe ◽  
Jian Liang Wu ◽  
Ryo Inoue ◽  
Minoru Fukiki ◽  
...  
Keyword(s):  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Vegf Expression ◽  
Cox 2

scholarly journals Differential expression and role of p21cip/waf1 and p27kip1 in TNF-α-induced inhibition of proliferation in human glioma cells

2007 ◽  
Vol 6 (1) ◽  
pp. 42 ◽  
Author(s):  
Pabbisetty Kumar ◽  
Anjali Shiras ◽  
Gowry Das ◽  
Jayashree C Jagtap ◽  
Vandna Prasad ◽  
...  
Keyword(s):  
Differential Expression ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Inhibition Of Proliferation ◽  
Tnf Α

scholarly journals Indirubin exerts anticancer effects on human glioma cells by inducing apoptosis and autophagy

AMB Express ◽  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhaohui Li ◽  
Han Wang ◽  
Jun Wei ◽  
Liang Han ◽  
Zhigang Guo
Keyword(s):  
Apoptotic Cell ◽  
Treatment Strategies ◽  
Glioma Cells ◽  
Annexin V ◽  
Metastatic Potential ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Efficient Treatment ◽  
Cell Percentage ◽  
Anticancer Effects

Abstract Glioma causes significant mortality across the world and the most aggressive type of brain cancer. The incidence of glioma is believed to increase in the next few decades and hence more efficient treatment strategies need to be developed for management of glioma. Herein, we examined the anticancer effects of Indirubin against a panel of human glioma cells and attempted to explore the underlying mechanisms. The results of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay showed that Indirubin could inhibit the growth of all the glioma cells but the lowest IC50 of 12.5 µM was observed against the U87 and U118 glioma cells. Additionally, the cytotoxic effects of Indirubin were comparatively negligible against the normal astrocytes with an IC50 of > 100 µM. Investigation of mechanism of action, revealed that Indirubin exerts growth inhibitory effects on the U87 and U118 glioma cells by autophagic and apoptotic cell death. Annexin V/PI staining assay showed that apoptotic cell percentage increased dose dependently. Apoptosis was associated with increase in Bax decrease in Bcl-2 expressions. Additionally, the expression of autophagic proteins such as LC3II, ATG12, ATG15 and Beclin 1 was also increased. Wound heal assay showed that Indirubin caused remarkable decrease in the migration of the U87 and U118 cells indicative of anti-metastatic potential of Indirubin. Taken together, these results suggest that Indirubin exerts potent anticancer effects on glioma cells and may prove essential in the management of glioma.

scholarly journals ROS-Mediated Cytotoxic Effect of Copper(II) Hydrazone Complexes against Human Glioma Cells

Molecules ◽  
2014 ◽  
Vol 19 (11) ◽  
pp. 17202-17220 ◽  
Author(s):  
Angel Recio Despaigne ◽  
Jeferson Da Silva ◽  
Pryscila da Costa ◽  
Raquel dos Santos ◽  
Heloisa Beraldo
Keyword(s):  
Cytotoxic Effect ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Effect Of Copper ◽  
Hydrazone Complexes
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