Ishii Masakazu, Oyama Akinori, Hagiwara Tamio, Miyazaki Akira, Mori Yasuo, Kiuchi Yuji, Shimizu Shunichi
Department of Pathophysiology, School of Pharmaceutical Sciences, Showa University, Shinagawa-ku, Tokyo 142-8555, Japan.
Anticancer Res. 2007 Nov-Dec;27(6B):3987-92.
The melastatin-like transient receptor potential M2 (TRPM2) channel is a Ca2+ permeable channel that is activated by reactive oxygen species (ROS), and its activation induces necrotic cell death. The effect of insertion of TRPM2 into A172 human glioblastoma cells (A172 cells) was investigated. The insertion of TRPM2 channels enhanced cell death induced by H2O2 in the A172 cells. An H2O2-induced Ca2+ increase was observed in TRPM2-expressing cells, but not in wild-type cells. Proliferation, migration and invasion activities were not affected by the expression of TRPM2. TRPM2 seems to be a candidate for gene therapy in glioblastoma cells, since the insertion of TRPM2 into A172 cells can facilitate cell death through Ca2+ increase after H2O2 treatment without increasing malignancy.
褪黑素样瞬时受体电位M2（TRPM2）通道是一种Ca2+通透通道，可被活性氧（ROS）激活，其激活会诱导坏死性细胞死亡。研究了将TRPM2插入A172人胶质母细胞瘤细胞（A172细胞）的效果。TRPM2通道的插入增强了H2O2诱导的A172细胞死亡。在表达TRPM2的细胞中观察到H2O2诱导的Ca2+增加，而在野生型细胞中未观察到。TRPM2的表达不影响增殖、迁移和侵袭活性。TRPM2似乎是胶质母细胞瘤细胞基因治疗的一个候选者，因为将TRPM2插入A172细胞可以在H2O2处理后通过增加Ca2+促进细胞死亡，而不会增加恶性程度。
