ERGIC3是转运蛋白，参与蛋白质从内质网到高尔基体的运输、分选和加工。经过系列筛选，我们在国际上首次发现ERGIC3在非小细胞肺癌（NSCLC）中异常高表达，且表达水平与肺癌组织学类型和分化程度相关；进一步证明ERGIC3促进肺癌细胞增殖和运动，且与表皮生长因子（EGF）、细胞周期蛋白cyclinD1有相互作用。但其分子机理不清楚。据此提出假说，ERGIC3促进肺癌细胞生长，可能通过运载相应细胞生长因子以调控细胞周期最关键的限制点（R点）信号通路cyclinD/E-Cdk而加速细胞生长，从而促进肺癌的发生发展。因此，本项目以细胞周期最关键的调控点--G1/S期关卡为突破口，研究ERGIC3表达变化与cyclinD/E-Cdk信号通路的关系，并用蛋白组学方法找出与ERGIC3相互作用的蛋白质，以期初步阐明ERGIC3异常表达在肺癌发生发展中的病理生理功能及其机制，为肺癌的防治提供实验依据。

ERGIC3 is a transporter and involved in protein sorting and transport from endoplasmic reticulum to Golgi complex and controls the cellular proliferation and movement. By the systematical screening, we found for the first time in the world that ERGIC3 was highly expressed in the non-small cell lung cancer (NSCLC), and the ERGIC3 level was linked to the histological types and differentiated degree of NSCLC. Further study shown that knock-down ERGIC3 could slow the cell growth and invasion in A549 cells, while over-expression of ERGIC3 could accelerate the cell growth and invasion in BEAS-2B cells. However, the mechanism is unclear. We propose hypothesis that ERGIC3 may transport some growth factors which regulate most important signal pathway of restriction point of cell cycle, that is cyclinD/E-Cdk pathway, then finally ERGIC3 controls the development and progression of NSCLC by promoting the cell oliferation. In this project, ① The most important signal pathway, cyclin D/E-Cdk at the R point will be selected in order to study its