RESUMEN
In recent years, with the deepening of tumor biology research, people have a newer and more comprehensive understanding of complex tumor metabolism reprogramming. The glucose transport protein-1(GLUT-1) is a glucose transporter widely expressed in the cell membranes of various tissues and represents unusual overexpression in the plasma membrane of virous cancer cell. GLUT-1 can transport man-nose, galactose, glucosamine and ascorbic acid (AA). GLUT-1 is overexpressed in different degrees on the plasma membrane of different tumor cells. Overexpressed GLUT-1 will make tumor cells take in more glucose to reprogram the metabolic mode of cells, and at the same time, it influences the change of tumor microenvironment. And the regulation of GLUT-1 in tumors has been the focus of attention in recent years, and the upstream regulators that have been reported mainly include phosphatase and tension homolog deleted on chromosome ten (PTEN) and hypoxia inducible factor (HIF). GLUT-1 also plays an important role in tumorigenesis and development by influencing the p53 and cellular tumorigenic gene (c-Myc) pathways. The review introduces structure and function of GLUT-1, the effects of transporting different substrates in tumor metabolic reprogramming, the regulation of GLUT-1, and the current treatment of GLUT-1. Meanwhile, the review discusses mechanisms and development of the role of GLUT-1 in cancer metabolism reprogramming, and points out the existing problems to provide reference for the research of metabolism reprogramming and targeted therapy of malignant tumors.
RESUMEN
Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) can effectively inhibit the growth of EGFR-dependent mutant non-small cell lung cancer (NSCLC). Unfortunately, NSCLC patients often develop severe drug resistance after long-term EGFR-TKI treatment. Studies have shown that the disorder of energy metabolism in tumor cells can induce EGFR-TKI resistance. Due to the drug action, gene mutation and other factors, tumor cells undergo metabolic reprogramming, which increases the metabolic rate and intensity of tumor cells, promotes the intake and synthesis of nutrients (such as sugar, fat and glutamine), forms a microenvironment conducive to tumor growth, enhances the bypass activation, phenotype transformation and abnormal proliferation of tumor cells, and inhibits the activity of immune cells and apoptosis of tumor cells, ultimately leading to drug resistance of tumor cells to EGFR-TKI. Therefore, targeting energy metabolism of NSCLC may be a potential way to alleviate TKI resistance.