EMT（上皮间质转化）和MET（间质上皮转化）在肿瘤转移中具有重要作用。申请者研究抗血管生成治疗后乳腺癌能量代谢的变化，发现高糖酵解乳腺癌对抗血管生成治疗药物反应更敏感，但却易发生继发转移瘤；发现高糖酵解乳腺癌肿瘤干细胞具有高表达。EMT能促进肿瘤细胞获得干细胞特性且使肿瘤细胞获得侵袭能力。肿瘤细胞如何逆转这种转化过程，生成具有上皮表型的转移灶？相对于EMT，MET的研究存在空白。申请者结合该现象设想，高糖酵解乳腺癌抗血管生成药物激活了MET，诱发高糖乳腺癌转移瘤发生，但机制有待深入研究。本项目应用FDG-PET靶向示踪高糖酵解，研究高糖酵解乳腺癌抗血管生成治疗后对原发癌、转移癌和循环血肿瘤细胞EMT与MET的影响；应用靶向示踪MET的11C-SU11274 PET显像，在体考察抗血管生成治疗后联合应用MET抑制剂能否抑制高糖酵解乳腺癌转移。研究结果有望为发现乳腺癌转移的新靶点提供依据。

The epithelial mesenchymal transition and mesenchymal epithelial transition play important roles in tumor progression. We evaluated the changes of energy metabolism in breast cancer after anti-angiogenic therapy by FDG PET, and found that high glycolytic breast cancer was more sensitive to therapy, but prone to metastasis. Further analysis revealed that the high glycolysis breast cancer had high cancer stem cell expression. EMT can promote tumor cell to obtain the characteristics of stem cell, and tumor cells lose their polarity and acquire the migration ability. How do mesenchymal phenotype cells reverse this transformation process, which generates a new metastatic lesion? Relative to the EMT, study on MET is few. Our hypothesis is that the antiangiogenic therapy activates the MET, however the mechanism need to be investigated. Our project would like to clarify EMT and MET characteristics in primary tumor, metastasis and circulating tumor cell after anti-angiogenic therapy. 11C-SU11274 PET imaging(targeted MET) is used to explore whether anti-angiogenic therapy combined with MET inhibitors can inhibit the metastasis of breast cancer with high glycolysis. The results are expected to find effective new target for breast cancer metastasis.