韩国科学家2月1日说，咖啡因可以抑制神经恶性肿瘤生长速度，抵御脑癌。

韩国科学技术院神经科专家李昌隽（音译）及其国际研究团队在美国《癌症研究》月刊发表论文说，动物实验显示，从普通咖啡和绿茶中提取的咖啡因可以有选择地阻止三磷酸肌醇受体活动，从而抑制神经胶质细胞肿瘤生长。

研究人员发现，脑癌患者体内三磷酸肌醇受体子型1，4，5－三磷酸肌醇受体相当活跃。咖啡因可有效阻止这种受体的活动，产生抑制肿瘤生长、防止癌细胞扩散的效果。

“这是科学家第一次发现咖啡因可以用于治疗神经胶质细胞肿瘤，”论文说。

李昌隽接受韩联社记者采访时说，实验中向动物注射的咖啡因剂量相当于喝茶或喝咖啡的人一天的咖啡因摄入量，大约为2至5杯咖啡或绿茶。

李昌隽指出，借助临床研究，科学家或许可将咖啡因运用至恶性脑瘤等癌症治疗中。

推荐原始出处：

Cancer Research 70, 1173, February 1, 2010. Published Online First January 26, 2010;

Caffeine-Mediated Inhibition of Calcium Release Channel Inositol 1,4,5-Trisphosphate Receptor Subtype 3 Blocks Glioblastoma Invasion and Extends Survival

Sang Soo Kang7, Kyung-Seok Han1,6, Bo Mi Ku7, Yeon Kyung Lee7, Jinpyo Hong5, Hye Young Shin3, Antoine G. Almonte8, Dong Ho Woo1,6, Daniel J. Brat8, Eun Mi Hwang7, Seung Hyun Yoo9, Chun Kee Chung3, Sung-Hye Park4, Sun Ha Paek3, Eun Joo Roh2, Sung joong Lee5, Jae-Yong Park7, Stephen F. Traynelis8 and C. Justin Lee1,6

Authors' Affiliations: 1 Center for Neural Science, Future Fusion Technology Laboratory; 2 Division of Life Sciences, Korea Institute of Science and Technology; Departments of 3 Neurosurgery and 4 Pathology, Cancer Research Institute, Clinical Research Institute, Seoul National University College of Medicine; 5 Program in Molecular and Cellular Neuroscience, Department of Oral Physiology, School of Dentistry, Seoul National University, Seoul, Republic of Korea; 6 Neuroscience Program, University of Science and Technology, Daejeon, Republic of Korea; 7 Department of Anatomy and Neurobiology, Department of Physiology, Institute of Health Sciences, School of Medicine, Gyeongsang National University, Jinju, Republic of Korea; 8 Department of Pharmacology, Emory University, Atlanta, Georgia; and 9 Department of Biochemistry, Inha University School of Medicine, Inchon, Republic of Korea

Calcium signaling is important in many signaling processes in cancer cell proliferation and motility including in deadly glioblastomas of the brain that aggressively invade neighboring tissue. We hypothesized that disturbing Ca2+ signaling pathways might decrease the invasive behavior of giloblastoma, extending survival. Evaluating a panel of small-molecule modulators of Ca2+ signaling, we identified caffeine as an inhibitor of glioblastoma cell motility. Caffeine, which is known to activate ryanodine receptors, paradoxically inhibits Ca2+ increase by inositol 1,4,5-trisphospate receptor subtype 3 (IP3R3), the expression of which is increased in glioblastoma cells. Consequently, by inhibiting IP3R3-mediated Ca2+ release, caffeine inhibited migration of glioblastoma cells in various in vitro assays. Consistent with these effects, caffeine greatly increased mean survival in a mouse xenograft model of glioblastoma. These findings suggest IP3R3 as a novel therapeutic target and identify caffeine as a possible adjunct therapy to slow invasive growth of glioblastoma.