Establishment and characterization of novel tumor cell migration factor, TRPV2 channel

新型肿瘤细胞迁移因子TRPV2通道的建立和表征

• 批准号: 20790247
• 负责人: NAKAGAWA Yuko
• 金额: $ 2.75万
• 依托单位: Gunma University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2009
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20790247/
• 关键词: がん; Ca^<2+>透過性チャネル; チャネル; カルシウム

The present study was conducted to characterize the regulation and function of TRPV2 channel in highly malignant tumor cell. The expression of TRPV2 was not only detected in the normal cell, but also in the tumor cell. We then determined localization of TRPV2 using metastatic B16 melanoma murine cells transfected with TRPV2-EGFP. In serum-free condition, most of the TRPV2 signal was located in the cytoplasm. Treatment with serum induced translocation of some of the TRPV2-EGFP to the plasma membrane. Serum-induced translocation was blocked by transfection of short-form TRPV2 (s-TRPV2) lacking a pore-forming region and the sixth transmembrane domain. These data conformed to that of macrophage TtT/M87 cell. To determine the function of migration for the TRPV2, we performed the wound healing assay. The ruthenium red, TRPV family inhibitor, blocked the migration of B6 cell. However s-TRPV2 couldn't inhibit the cell migration.

进行了本研究以表征高度恶性肿瘤细胞中TRPV2通道的调节和功能。不仅在正常细胞中，而且在肿瘤细胞中检测到TRPV2的表达。然后，我们使用用TRPV2-EGFP转染的转移性B16黑色素瘤细胞确定了TRPV2的定位。在无血清条件下，大多数TRPV2信号位于细胞质中。用血清诱导的一些TRPV2-EGFP易位到质膜。血清诱导的易位通过缺乏孔形成区域和第六个跨膜结构域的短形式TRPV2（S-TRPV2）的转染来阻断。这些数据符合巨噬细胞TTT/M87细胞的数据。为了确定TRPV2迁移的功能，我们进行了伤口愈合测定法。 TRPV家族抑制剂Ruthenium Red阻止了B6细胞的迁移。但是，S-TRPV2无法抑制细胞迁移。

项目成果

膵β細胞における甘味感受体T1R2+T1R3の機能解析

胰腺β细胞甜味受体T1R2+T1R3的功能分析

• 发表时间: 2009
• 作者: 中川祐子;原朱美;長澤雅裕;最上秀夫;小島至
• 通讯作者: 小島至

Sweet taste receptor expressed in pancreatic beta-cells activates the calcium and cyclic AMP signaling systems and stimulates insulin secretion.

• DOI: 10.1371/journal.pone.0005106
• 发表时间: 2009
• 期刊: PloS one
• 影响因子: 3.7
• 作者: Nakagawa Y;Nagasawa M;Yamada S;Hara A;Mogami H;Nikolaev VO;Lohse MJ;Shigemura N;Ninomiya Y;Kojima I
• 通讯作者: Kojima I