MicroRNAs play an important role in tumor development and progression. Tumor growth is closely associated with glucose metabolism. Specifically, tumor cells produce energy (ATP) under aerobic and anaerobic conditions through glycolysis and metabolites, such as lactic acid and ATP, as a result of the Warburg effect. However, the transport of glucose into cells depends on protein transporters in the cell membrane. Therefore, this area has recently become a topic of interest for research on targeted cancer therapy. We found that miRNA-451 inhibits the phosphatidylinositol-3 kinase (PI3K)/Akt signaling pathway to modify the biological behavior of glioma cells. Inhibiting the PI3K/Akt pathway may prevent glucose-addicted cancer cells from performing glycolysis. Akt directly affects glycolysis by regulating the localization of the glucose transporter 1 (GLUT1). However, how miRNA-451 regulates glucose transporters on the cell membrane and affects the regulatory mechanisms of glucose metabolism in glioma cells remains unclear. Consequently, we predict and verify related gene protein interactions. By targeting CAB 39, miRNA-451 likely triggers the LKB1/AMPK/PI3K/AKT pathway, which regulates GLUT1, to inhibit the glucose metabolism of, reduce the energy supply to, and inhibit the proliferation and invasion of glioma cells. Our results suggest a new direction for the treatment of glioma.

译文

microrna在肿瘤的发展和进展中起重要作用。肿瘤生长与葡萄糖代谢密切相关。具体来说,由于Warburg效应,肿瘤细胞在有氧和厌氧条件下通过糖酵解和代谢产物 (例如乳酸和ATP) 产生能量 (ATP)。然而,葡萄糖向细胞的转运取决于细胞膜中的蛋白质转运蛋白。因此,该领域最近成为靶向癌症治疗研究的兴趣话题。我们发现miRNA-451抑制phosphatidylinositol-3激酶 (PI3K)/Akt信号通路来改变神经胶质瘤细胞的生物学行为。抑制PI3K/Akt途径可能会阻止葡萄糖成瘾的癌细胞进行糖酵解。Akt通过调节葡萄糖转运蛋白1 (GLUT1) 的定位直接影响糖酵解。然而,miRNA-451如何调节细胞膜上的葡萄糖转运蛋白并影响神经胶质瘤细胞中葡萄糖代谢的调节机制仍不清楚。因此,我们预测并验证了相关的基因蛋白相互作用。通过靶向CAB 39,miRNA-451可能会触发LKB1/AMPK/PI3K/AKT途径,该途径调节GLUT1,以抑制其葡萄糖代谢,减少能量供应并抑制神经胶质瘤细胞的增殖和侵袭。我们的结果为神经胶质瘤的治疗提供了新的方向。

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