钙离子是细胞内调节细胞细胞增殖、分化、基因转录、信号转导等生命活动的重要第二信使。STIM1 和 Orai1介导的钙池操纵的钙内流(store-operated calcium entry, SOCE)是由非兴奋细胞（包括大多数癌症细胞）调节Ca2+稳态平衡的重要途径。侵袭伪足是细胞进行侵袭性迁移所特化的结构，在肿瘤细胞侵袭迁移过程中发挥重要作用。前期研究表明，SOCE通过影响Src的活性和MT1-MMP的亚细胞定位来调控侵袭伪足的形成和功能，但其中的分子机制仍然在很大程度上是未知的。本研究拟从细胞生物学、生物化学角度详细阐述STIM1 介导的钙离子流入调控侵袭伪足形成的分子机制。研究结果将有助于诠释STIM1和Orai1促进侵袭性转移的分子机制，提供了钙离子介导的肿瘤细胞侵袭转移一种新的机制。对侵袭转移机制的深入研究及提供潜在的新的癌症药物治疗靶标具有重要的指导意义。

Ca2+ acts as a universal and versatile second messenger in the regulation of a myriad of biological processes, including cell proliferation, differentiation, gene transcription and signal transduction et al. In non-excitable cells, STIM1 and Orai1 mediated SOCE is the predominant Ca2+ entry mechanism, which is activated when intracellular stores, such as endoplasmic reticulum (ER), release their stored Ca2+. Invadopodia is specialized structure that promotes.migration and invasion in cancer cells. We have shown that SOCE affect invadopodia formation and function through regulation of Src activity and the subcellular localization of MT1-MMP, but the detailed mechanism remain largely unknown, Here we will elaborate how SOCE affect invadopodia formation through cell biology and biochemistry in this study, our result will offer molecular mechanism how SOCE promote metastasis and potential drug target for cancer therapy.