作者: KYUNG-HO JUNG , JIN HEE LEE , JIN WON PARK , SEUNG-HWAN MOON , YOUNG SEOK CHO
DOI: 10.3892/OR.2015.4460
关键词: Cancer cell 、 Cell biology 、 Cell 、 Glycolysis 、 Intracellular 、 Biology 、 Curcumin 、 PI3K/AKT/mTOR pathway 、 Apoptosis 、 Mitochondrion
摘要: A better understanding of how curcumin influences cancer cell biology could help devise new strategies to enhance its antitumor effect. Many actions are proposed occur by targeting mitochondrial function, among which glucose metabolism and reactive oxygen species (ROS) production pivotal. However, little is known metabolism. We thus evaluated the effect on further investigated whether these responses be modified anticancer potency compound. MCF-7 breast cells treated with were measured for 18F-fluorodeoxyglucose (18F‑FDG) uptake, lactate production, hexokinase activity, consumption rate (OCR), ROS membrane potential (MMP). Activation signaling pathways was western blots, survival assessed sulforhodamine B assays. Curcumin stimulated a 3.6-fold increase 18F-FDG uptake in cells, along augmented activity efflux. This accompanied significantly suppressed cellular OCR, consistent metabolic shift glycolytic flux. Inhibiting this response 2-deoxyglucose (2-DG) blocked curcumin-induced mTOR activation resulted greater anti-proliferative Curcumin-induced MMP depolarization led reduced may hinder Intracellular completely restored adding Cu2+, can bind modify curcumin's physico-chemical property, marked potentiation Thus, suppresses generation, via shifting from respiration These provide targets that action curcumin.