Title | Expression of eIF4E Gene in Glioma and Its Sensitivity to Oxidative Stress |
Author | |
Publication Years | 2022
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DOI | |
Source Title | |
ISSN | 1942-0900
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EISSN | 1942-0994
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Volume | 2022 |
Abstract | Objective: Increased expression of eIF4E has been observed in various cancers, which makes eIF4E an attractive target of anticancer drugs. This study mainly discussed eIF4E gene expression in glioma and its sensitivity to oxidative stress (OS). Methods: Relevant data from The Cancer Genome Atlas (TCGA) database regarding eIF4E gene expression and its prognostic significance in glioma samples were analyzed. Additionally, we measured eIF4E at mRNA and protein levels in clinical samples collected between July 2019 and September 2021, as well as glioma cell strains. U251 cells cultured in vitro were treated with OS injury induced by hydrogen peroxide (H2O2) and then transfected with si-eIF4E to determine changes in cell multiplication, invasiveness, and migration capacities as well as apoptosis rate. ELISA quantified cell malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) concentrations, and flow cytometry measured reactive oxygen species (ROS) level. Results: In glioma samples from the TCGA database, eIF4E showed obviously elevated levels in LGG and GBM patients, which was usually associated with adverse patient prognosis (P < 0.05). eIF4E was also upregulated in glioma cell strains than in HBE cells. In comparison with the blank control group, transfection of si-eIF4E statistically suppressed the capacity of U251 cells to proliferate, invade and migrate, and enhance apoptosis rate, while reducing SOD and GSH-Px and increasing MDA and ROS. In addition, H2O2 induced the upregulation of eIF4E in U251 cells. H2O2 + si-eIF4E exhibited reduced multiplication and number of clone cell formation, invasion, and migration of U251 cells, as well as increased apoptosis rate than H2O2 + si-NC group. Conclusions: eIF4E is highly expressed in glioma. Knocking down eIF4E can effectively inhibit the capacity of U251 to proliferate, invade and migrate, and significantly increase apoptosis. In addition, eIF4E knock-down is able to lower OS reaction under H2O2 inducement and enhance U251 cells' sensitivity to OS. |
URL | [Source Record] |
Indexed By | |
Language | English
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SUSTech Authorship | First
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Funding Project | [GJHZ20190821161601670]
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WOS Research Area | Cell Biology
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WOS Subject | Cell Biology
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WOS Accession No | WOS:000869967200008
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Publisher | |
Scopus EID | 2-s2.0-85139798417
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Data Source | Scopus
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Citation statistics |
Cited Times [WOS]:1
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Document Type | Journal Article |
Identifier | http://kc.sustech.edu.cn/handle/2SGJ60CL/406607 |
Department | Shenzhen People's Hospital 南方科技大学医学院 |
Affiliation | 1.Department of Neurosurgery, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, Guangdong 518020, China 2.First Clinical Medical College of Jinan University,Jinan University,Guangzhou,510630,China 3.School of Medicine,Southern University of Science and Technology,Shenzhen,518055,China 4.Department of Neurosurgery,Shenzhen Luohu Hospital Group,Third Affiliated Hospital of Shenzhen University,Shenzhen,518001,China 5.Neurosurgery Department of School of Medicine,Chinese University of Hong Kong,Shenzhen,518172,China |
First Author Affilication | Shenzhen People's Hospital |
First Author's First Affilication | Shenzhen People's Hospital |
Recommended Citation GB/T 7714 |
Liang,Jian,Yang,Yaoqiang,Li,Xing,et al. Expression of eIF4E Gene in Glioma and Its Sensitivity to Oxidative Stress[J]. Oxidative Medicine and Cellular Longevity,2022,2022.
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APA |
Liang,Jian,Yang,Yaoqiang,Li,Xing,Cai,Guangmou,Cao,Jianxuan,&Zhang,Bo.(2022).Expression of eIF4E Gene in Glioma and Its Sensitivity to Oxidative Stress.Oxidative Medicine and Cellular Longevity,2022.
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MLA |
Liang,Jian,et al."Expression of eIF4E Gene in Glioma and Its Sensitivity to Oxidative Stress".Oxidative Medicine and Cellular Longevity 2022(2022).
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