目的 探究流体剪切力（fluid shear stress, FSS）对喉鳞癌Hep2细胞发生上皮-间充质转化（epithelial mesenchymal transition，EMT）的影响。方法 对Hep2细胞加载140 mPa的FSS，观察不同时间点细胞的形态学变化；划痕实验检测力学加载后Hep2细胞迁移能力的变化；共聚焦显微镜下观察细胞骨架蛋白F-actin的分布；Western blotting检测EMT相关蛋白的表达。结果 FSS力学加载后，Hep2细胞形态由多边形向梭形转变，撤销FSS后，细胞恢复初始的多边形；Hep2细胞迁移能力的增加依赖于FSS加载时间。FSS促使细胞骨架蛋白F-actin重排，从而增强Hep2细胞的迁移行为。FSS使Hep2细胞EMT标志蛋白发生了时序性变化。结论 FSS是诱导Hep2细胞发生EMT的一个重要物理因素。

Objective To examine the effects of fluid shear stress (FSS) on epithelial-mesenchymal transition (EMT) in Hep2 cells. Methods Hep2 cells were exposed to 140 mPa FSS. The morphologic changes of Hep2 cells exposed to FSS at different durations were observed using inverted microscope. The migration ability of Hep2 cells after FSS loading was investigated using scratch wound assay. The distribution and expression of cytoskeleton protein F-actin were examined by confocal microscope. The expression of the EMT marker proteins were detected by Western blotting. Results Most of Hep2 cells changed their morphology from polygon to elongated spindle with well-organized F-actin under FSS. After removing FSS, Hep2 cells recovered their initial morphology with flat polygon. FSS regulated Hep2 cells to enhance their migration capacity in a time-dependent manner. FSS promoted the rearrangement of cytoskeletal protein F-actin，which enhanced the migration behavior of Hep2 cells. In addition, FSS induced a time regularity of expression of the EMT marker proteins in Hep2 cells. Conclusions FSS as an important physical factor can induce EMT in Hep2 cells.

国家自然科学基金项目（11172189，11372203）