目的:检测Caveolin-1 蛋白（Cav-1）对胃癌（gastric cancer，GC）细胞株NCI-N87 恶性生物学行为的影响及其可能的作用机制。方法：构建Cav-1 过表达稳转染细胞系N87/Cav-1，应用MTT、克隆形成、划痕修复实验检测Cav-1 对胃癌细胞株NCIN87恶性生物学行为的影响，应用Western blotting 检测在EGF配体诱导下Cav-1 蛋白对Her-2 活化及ERK、Akt 信号通路的影响。结果：Cav-1 过表达可明显抑制胃癌细胞NCI-N87 的增殖及迁移能力；在配体EGF刺激下，Cav-1 过表达明显抑制了Her-2 酪氨酸磷酸化水平以及P-ERK/ERK、P-AKT/AKT的比率（P<0.01）。结论：Cav-1 过表达可明显抑制EGF诱导的Her-2 酪氨酸磷酸化水平，并可能通过下游MAPK及PI3K/Akt 信号通路的作用抑制了胃癌细胞株NCI-N87 的增殖及迁移能力。

Objective: To investigate the effect of Caveolin-1(Cav-1) protein on the malignant biological behaviors of NCI-N87 gastric cancer cells, and further to analyze the possible molecular mechanisms. Methods: NCI-N87 cell line that stably expressing Cav-1 was constructed; MTT assay, colony formation assay and wound healing assay were used to examine the effect of Cav-1 on the malignant biological behaviors of gastric cancer cells; Western bloting was used to detect the effect of Cav-1 protein on Her-2 activation as well as the ERK and Akt signaling pathway under the induction with EGF ligand. Results: Over-expression of Cav-1 significantly inhibited the proliferation and migration of NCI-N87 cells. With the stimulation of EGF ligand, Cav-1 over-expression significantly inhibited the tyrosine phosphorylation level of Her-2 and the ratio of P-ERK/ERK as well as P-AKT/AKT. Conclusion: The over-expression of Cav-1 could significantly inhibit Her-2 tyrosine phosphorylation, and may inhibit the proliferation and migration of NCI-N87 cells via the down-stream MAPK and PI3K/Akt signaling pathway.

国家自然科学基金资助项目(No. 81071846)；吴阶平医学基金资助项目(No.320.6750.14063)；河北省医学科学研究重点课题计划项目（No. 20170698）