Functional importance of glucose transporters and chromatin epigenetic factors in Glioblastoma Multiforme (GBM): possible therapeutics

被引:7
|
作者
Chamarthy, Sahiti [1 ]
Mekala, Janaki Ramaiah [1 ]
机构
[1] Koneru Lakshmaiah Educ Fdn KLEF, Dept Biotechnol, Guntur 522302, Andhra Pradesh, India
关键词
GLUT-1; GLUT-3; GBM; miRs; BBB; Palmitoylation; PYRUVATE-KINASE M2; CENTRAL-NERVOUS-SYSTEM; TARGETING HEXOKINASE 2; LONG NONCODING RNAS; CELL-PROLIFERATION; BREAST-CANCER; REGULATES GLYCOLYSIS; TUMOR-SUPPRESSOR; SKELETAL-MUSCLE; CYTOCHALASIN B;
D O I
10.1007/s11011-023-01207-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Glioblastoma Multiforme (GBM) is an aggressive brain cancer affecting glial cells and is chemo- and radio-resistant. Glucose is considered the most vital energy source for cancer cell proliferation. During metabolism, hexose molecules will be transported into the cells via transmembrane proteins known as glucose transporter (GLUT). Among them, GLUT-1 and GLUT-3 play pivotal roles in glucose transport in GBM. Knockdown studies have established the role of GLUT-1, and GLUT-3 mediated glucose transport in GBM cells, providing insight into GLUT-mediated cancer signaling and cancer aggressiveness. This review focussed on the vital role of GLUT-1 and GLUT-3 proteins, which regulate glucose transport. Recent studies have identified the role of GLUT inhibitors in effective cancer prevention. Several of them are in clinical trials. Understanding and functional approaches towards glucose-mediated cell metabolism and chromatin epigenetics will provide valuable insights into the mechanism of cancer aggressiveness, cancer stemness, and chemo-resistance in Glioblastoma Multiforme (GBM). This review summarizes the role of GLUT inhibitors, micro-RNAs, and long non-coding RNAs that aid in inhibiting glucose uptake by the GBM cells and other cancer cells leading to the identification of potential therapeutic, prognostic as well as diagnostic markers. Furthermore, the involvement of epigenetic factors, such as microRNAs, in regulating glycolytic genes was demonstrated.
引用
收藏
页码:1441 / 1469
页数:29
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