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

本研究旨在探讨TRPV 2通道在高度恶性肿瘤细胞中的调控和功能。TRPV 2不仅在正常细胞中表达，而且在肿瘤细胞中也有表达。然后，我们使用用TRPV 2-EGFP转染的转移性B16黑色素瘤鼠细胞确定TRPV 2的定位。在无血清条件下，TRPV 2信号主要位于细胞质中。用血清处理诱导一些TRPV 2-EGFP易位至质膜。通过转染缺乏成孔区和第六跨膜结构域的短型TRPV 2（s-TRPV 2）可以阻断血清诱导的易位。这些数据与巨噬细胞TtT/M87细胞的结果一致。为了确定TRPV 2的迁移功能，我们进行了伤口愈合测定。TRPV家族抑制剂钌红可阻断B6细胞的迁移。而s-TRPV 2不能抑制细胞的迁移。

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.