The role of TRPV2 channel trafficking in cancer cell adhesion and motility

TRPV2通道在多种癌细胞中表达。本研究选择人纤维肉瘤细胞系作为模型系统。EGF刺激通过磷脂酰肌醇（PI） 3激酶依赖机制诱导TRPV2易位至质膜。此外，EGF的应用引起细胞质钙的持续增加。TRPV2或TRP抑制剂的下调阻断了游离钙浓度的变化。TRPV2定位于细胞的丝状足或板足。TRPV2还可与β-整合素、paxiliin和vinculin等黏附结构共定位。为了进一步分析这些TRPV2的定位，我们使用了血管蛋白构象传感器FRET探针或血管蛋白张力传感器FRET探针。在迁移细胞的前部周围观察到血管蛋白构象的改变和钙离子的改变。TRPV2的转运与质膜的再循环有关。

TRPV2 channel was expressed in various cancer cells. In the present study, human fibrosarcoma cell lines was selected as a model system. Stimulation by EGF induced translocation of TRPV2 to the plasma membrane by a phosphatidylinositol (PI) 3-kinase-dependent mechanism. Moreover, an application of EGF caused a sustained increase of cytoplasmic calcium. Knock down of TRPV2 or TRP inhibitors blocked the changes in free calcium concentration. TRPV2 was localized at the filopodia or lamellipodia in the cells. TRPV2 also colocalized with focal adhesion structures, such as β-integrin, paxiliin, and vinculin. To further analyze these localization of TRPV2, vinculin conformation sensor FRET probe or vinculin tension sensor FRET probe was used. The vinculin conformation changes and calcium changes were observed around the front of the migrating cells. TRPV2 trafficking is related with the recycling of the plasma membrane.