作者: Federico S. Rodríguez , Katterine A. Salazar , Nery A. Jara , María A García-Robles , Fernando Pérez
DOI: 10.1111/JNC.12365
关键词: Biology 、 GLUT1 、 Biochemistry 、 Vitamin C 、 Extracellular 、 Dehydroascorbic acid 、 Cancer research 、 Ascorbic acid 、 Glioma 、 Bystander effect 、 Microglia
摘要: Glioblastomas are lethal brain tumors that resist current cytostatic therapies. Vitamin C may antagonize the effects of reactive oxygen species (ROS) generating therapies; however, it is often used to reduce therapy-related side despite its on therapy or tumor growth. Because mechanisms vitamin uptake in gliomas currently unknown, we evaluated expression sodium-vitamin cotransporter (SVCT) and facilitative hexose transporter (GLUT) families human glioma cells. In addition, as microglial cells can greatly infiltrate high-grade (constituting up 45% glioblastomas), effect TC620 cell interactions with microglial-like HL60 (Bystander effect) was determined. Although expressed high levels SVCT isoform-2 (SVCT2), low functional activity, intracellular localization dominant-negative isoform (dnSVCT2) were observed. The increased glucose metabolic activity evident by 2-Deoxy-d-glucose dehydroascorbic acid (DHA) rates through GLUT isoform-1 (GLUT1), main DHA glioblastoma. Co-culture activated resulted extracellular ascorbic oxidation This Bystander explain antioxidative potential observed gliomas. study strongly suggests effect, is, interaction oxidant-producing microglia, could be an important mechanism for loading absence 2 (SVCT2) expression. cellular load results from a generated neighboring microglia. gliomas, considering only neoplasm where microglia almost equal number