题名 | GBE1 Promotes Glioma Progression by Enhancing Aerobic Glycolysis through Inhibition of FBP1 |
作者 | |
发表日期 | 2023-03 |
发表期刊 | CANCERS 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Article |
关键词 | glucan branching enzyme 1 Warburg effect glucose metabolism fructose-bisphosphatase 1 NF-kappa B |
其他关键词 | COMPETITION |
摘要 | Simple Summary: Due to the poor prognosis of glioma patients and the limitations of glioma treatment, our study aimed to find new targets for glioma on metabolic therapy. Our study reveals a role for glycogen branching enzyme 1 (GBE1) in regulating glioma initiation and progression. We found that the expression of GBE1 correlated with a poor prognosis in glioma patients. Moreover, GBE1 promotes glioma progression by enhancing aerobic glycolysis through the inhibition of fructose-bisphosphatase 1 (FBP1), which reveals GBE1 as a potential target for glioma therapy. Tumor metabolism characterized by aerobic glycolysis makes the Warburg effect a unique target for tumor therapy. Recent studies have found that glycogen branching enzyme 1 (GBE1) is involved in cancer progression. However, the study of GBE1 in gliomas is limited. We determined by bioinformatics analysis that GBE1 expression is elevated in gliomas and correlates with poor prognoses. In vitro experiments showed that GBE1 knockdown slows glioma cell proliferation, inhibits multiple biological behaviors, and alters glioma cell glycolytic capacity. Furthermore, GBE1 knockdown resulted in the inhibition of the NF-kappa B pathway as well as elevated expression of fructose-bisphosphatase 1 (FBP1). Further knockdown of elevated FBP1 reversed the inhibitory effect of GBE1 knockdown, restoring glycolytic reserve capacity. Furthermore, GBE1 knockdown suppressed xenograft tumor formation in vivo and conferred a significant survival benefit. Collectively, GBE1 reduces FBP1 expression through the NF-kappa B pathway, shifting the glucose metabolism pattern of glioma cells to glycolysis and enhancing the Warburg effect to drive glioma progression. These results suggest that GBE1 can be a novel target for glioma in metabolic therapy. |
资助项目 | National Natural Science Foundation of China [82103216, 81820108011, 82271345]; Zhejiang Provincial Natural Science Foundation of China [LQ20H090005] |
出版者 | MDPI |
ISSN | 2072-6694 |
EISSN | 2072-6694 |
卷号 | 15期号:5 |
DOI | 10.3390/cancers15051594 |
页数 | 20 |
WOS类目 | Oncology |
WOS研究方向 | Oncology |
WOS记录号 | WOS:000948083900001 |
收录类别 | SCIE ; SCOPUS ; PUBMED |
URL | 查看原文 |
PubMed ID | 36900384 |
SCOPUSEID | 2-s2.0-85149822167 |
通讯作者地址 | [Zhuge, Qichuan]Zhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China ; [Xia, Lei]Zhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China |
Scopus学科分类 | Oncology;Cancer Research |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/174648 |
专题 | 附属第一医院 第一临床医学院(信息与工程学院)、附属第一医院_中心实验室 |
通讯作者 | Zhuge, Qichuan; Xia, Lei |
作者单位 | 1.Zhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China; 2.Department of Neurosurgery,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China; 3.Central Laboratory,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China |
第一作者单位 | 附属第一医院; 第一临床医学院(信息与工程学院)、附属第一医院 |
通讯作者单位 | 附属第一医院; 第一临床医学院(信息与工程学院)、附属第一医院 |
第一作者的第一单位 | 附属第一医院 |
推荐引用方式 GB/T 7714 | Chen, Zhen,Bao, Han,Long, Jingfang,et al. GBE1 Promotes Glioma Progression by Enhancing Aerobic Glycolysis through Inhibition of FBP1[J]. CANCERS,2023,15(5). |
APA | Chen, Zhen., Bao, Han., Long, Jingfang., Zhao, Peiqi., Hu, Xiaowei., ... & Xia, Lei. (2023). GBE1 Promotes Glioma Progression by Enhancing Aerobic Glycolysis through Inhibition of FBP1. CANCERS, 15(5). |
MLA | Chen, Zhen,et al."GBE1 Promotes Glioma Progression by Enhancing Aerobic Glycolysis through Inhibition of FBP1".CANCERS 15.5(2023). |
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