肿瘤细胞发生EMT并定向迁移是肿瘤侵袭转移的重要环节。Caveolin-1（Cav1）能促使肿瘤细胞发生EMT并增强侵袭性，但具体机制仍待深入研究。既往研究表明，Cav1通过调控STAT3信号在肺癌细胞增殖中发挥作用，我们进一步研究发现发生EMT后肺癌细胞Cav1和磷酸化STAT3表达增高，迁移加快，侵袭增强。而且，定向迁移的肺癌细胞中，Cav1在前进一侧出现极化分布，STAT3则显著磷酸化并发生核转位。干扰Cav1表达后侵袭和迁移减弱，EMT关键分子Snail表达下调。由此，我们提出"Caveolin-1可能通过活化STAT3调控肺癌细胞发生EMT和定向迁移，进而促进肺癌的侵袭转移"。本研究拟在建立肺癌细胞定向迁移模型基础上，以"Caveolin-1和STAT3活化"的相互关系为切入点，探讨调控肺癌细胞EMT和定向迁移的新机制，为寻找阻断肺癌侵袭转移的关键分子靶点提供新的思路和实验依据。

Epithelial-to-Mesenchymal Transition (EMT) and directional migration are key steps in cancer invasion and metastasis. Caveolin-1 was reported to promote EMT and cancer invasion, but the underlying mechanisms are not fully understood. Based on previous reports that caveolin-1 regulates lung cancer cell proliferation through activation of STAT3, we invesgated the role of caveolin-1 and STAT3 in directional migration of lung cancer cells. We found that lung cancer cells displayed increased caveolin-1 and pSTAT3 expression, increased motility and invasiveness after EMT. Moreover, caveolin-1 accumulated at the leading edge of directionally migrating cells, while pSTAT3 expression increased significantly and displayed neuclear translocation. Moreover, siRNA-knockdown of caveolin-1 decreased cellular motility, invasiveness, as well as expression of an EMT regulator, Snail. Based on these results, we hypothesized that "Caveolin-1 regulates EMT and directioanl migration of lung cancer cells through activation of STAT3". Using a directional-cell-migration model, we aim to study new mechanisms controling EMT and directioanl migration of lung cancer cells, focsing on relationship between Caveolin-1 and STAT3 activation. We will provide new insights and experimental evidence for mechanisms controling lung cancer invasion and metastasis.