EMT与肿瘤转移关系密切。关于肿瘤转移过程中的“可逆性EMT理论”,近期得到一些实验证据的支持。但是,有哪些基因可以作为调控肿瘤转移过程中EMT或MET的分子开关?其调控机制有哪些?这些科学问题尚待解决。我们的前期研究已经初步证实GTP酶活化蛋白Git2与乳腺癌转移过程中EMT或MET作用有关。本项目拟进一步探讨Git2基因调控乳腺癌细胞EMT或MET的分子机制以及该调控作用介导肿癌转移的启动或克隆形成的机理。本项目的实施不但可以进一步完善肿瘤转移过程中“可逆性EMT理论”的理论体系,而且对乳腺癌转移的诊断和治疗也具有一定指导意义。

EMT was a critical process during cancer metastasis. Recently, more and more evidence supported the “reversal EMT theory” on several published research papers. However, which genes can switch EMT or MET and how these genes regulate EMT or MET during cancer metastasis are still obscure. Our preliminary data demonstrated that GTPase activating protein Git2 was involved into regulation of EMT or MET in several special breast cancer cells. On this project, we plan to investigate the molecular mechanism of Git2 mediated EMT or MET and how they regulate breast cancer metastatic initiation and colonization. The study should lead to an increased understanding of “reversal EMT theory” for cancer metastasis and suppose to slash a novel guidance for diagnose and therapy of breast cancer metastasis.