Differences in accumulation and the transport mechanism of l- and d-methionine in high- and low-grade human glioma cells

2017 ◽  
Vol 44 ◽  
pp. 78-82 ◽  
Author(s):  
Masato Kobayashi ◽  
Asuka Mizutani ◽  
Kodai Nishi ◽  
Syuichi Nakajima ◽  
Naoto Shikano ◽  
...  
Keyword(s):  
Transport Mechanism ◽  
Glioma Cells ◽  
Low Grade ◽  
Human Glioma ◽  
Human Glioma Cells

TAMI-47. MIR-542-3P CONTRIBUTES TO THE HK2-MEDIATED HIGH GLYCOLYTIC PHENOTYPE IN HUMAN GLIOMA CELLS

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi208-vi208
Author(s):  
Junhyung Kim ◽  
Min Woo Park ◽  
Ju Won Ahn ◽  
Jeong Min Sim ◽  
Suwan Kim ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Cellular Proliferation ◽  
Glioma Cells ◽  
Low Grade ◽  
High Grade ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Glycolytic Activity ◽  
High Grade Gliomas ◽  
Glycolytic Phenotype

Abstract BACKGROUND The elevation of glucose metabolism is linked to high-grade gliomas such as glioblastoma multiforme (GBM). The high glycolytic phenotype is associated with cellular proliferation and resistance to treatment with chemotherapeutic agents in GBM. MicroRNA-542-3p (miR-542-3p) has been implicated in several tumors including gliomas. However, the role of miR-542-3p in glucose metabolism in human gliomas remains unclear. METHODS We measured the levels of cellular proliferation in human glioma cells. We measured the glycolytic activity in miR-542-3p knockdown and over-expressed human glioma cells. We measured the levels of miR-542-3p and HK2 in glioma tissues from patients with low- and high-grade gliomas using imaging analysis. RESULTS We show that knockdown of miR-542-3p significantly suppressed cellular proliferation in human glioma cells. Knockdown of miR-542-3p suppressed HK2-induced glycolytic activity in human glioma cells. Consistently, over-expression of miR-542-3p increased HK2-induced glycolytic activity in human glioma cells. The levels of miR-542-3p and HK2 were significantly elevated in glioma tissues of patients with high-grade gliomas relative to that in low-grade gliomas. The elevation of HK2 levels in patients with high-grade gliomas were positively correlated with the high levels of miR-542-3p in GBM and low-grade gliomas (LGG) based on the datasets from the Cancer Genome Atlas (TCGA) database. Moreover, the high levels of miR-542-3p were associated with poor survival rate in the TCGA database. CONCLUSIONS miR-542-3p contributes to the HK2-mediated high glycolytic phenotype in human glioma cells.

scholarly journals miR-542-3p Contributes to the HK2-Mediated High Glycolytic Phenotype in Human Glioma Cells

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 633
Author(s):  
Junhyung Kim ◽  
Min Woo Park ◽  
Young Joon Park ◽  
Ju Won Ahn ◽  
Jeong Min Sim ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Cellular Proliferation ◽  
Glioma Cells ◽  
Low Grade ◽  
High Grade ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Glycolytic Activity ◽  
High Grade Gliomas ◽  
Glycolytic Phenotype

(1) Background: The elevation of glucose metabolism is linked to high-grade gliomas such as glioblastoma multiforme (GBM). The high glycolytic phenotype is associated with cellular proliferation and resistance to treatment with chemotherapeutic agents in GBM. MicroRNA-542-3p (miR-542-3p) has been implicated in several tumors including gliomas. However, the role of miR-542-3p in glucose metabolism in human gliomas remains unclear; (2) Methods: We measured the levels of cellular proliferation in human glioma cells. We measured the glycolytic activity in miR-542-3p knockdown and over-expressed human glioma cells. We measured the levels of miR-542-3p and HK2 in glioma tissues from patients with low- and high-grade gliomas using imaging analysis; (3) Results: We show that knockdown of miR-542-3p significantly suppressed cellular proliferation in human glioma cells. Knockdown of miR-542-3p suppressed HK2-induced glycolytic activity in human glioma cells. Consistently, over-expression of miR-542-3p increased HK2-induced glycolytic activity in human glioma cells. The levels of miR-542-3p and HK2 were significantly elevated in glioma tissues of patients with high-grade gliomas relative to that in low-grade gliomas. The elevation of HK2 levels in patients with high-grade gliomas were positively correlated with the high levels of miR-542-3p in GBM and low-grade gliomas (LGG) based on the datasets from the Cancer Genome Atlas (TCGA) database. Moreover, the high levels of miR-542-3p were associated with poor survival rate in the TCGA database; (4) Conclusions: miR-542-3p contributes to the HK2-mediated high glycolytic phenotype in human glioma cells.

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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