雌激素是女性体内的主要性激素，在女性生殖系统和乳腺生长发育及生理功能调节中发挥重要作用，但异常情况下雌激素则是促进乳腺癌恶性进展的重要因素。新近发现雌激素新受体G蛋白偶联受体30（GPR30）与乳腺癌侵袭和转移关系密切，但其信号机制尚不清楚。我们尝试提出"GPR30-钙激活中性蛋白酶（CANP）-黏着斑激酶（FAK）信号通路可能调控乳腺癌侵袭和转移"的假设。为此，本项目拟采用现代生物学研究手段，在细胞及分子水平观察GPR30对CANP系统的影响及CANP与FAK的相互作用，以了解GPR30-CANP-FAK信号通路的调节，并探讨该通路在乳腺癌细胞侵袭等恶性生物学行为中的作用；通过裸鼠乳腺癌转移模型实验，在整体水平验证上述实验结果，以期发现GPR30通路中调控肿瘤转移的关键分子，加深对雌激素促进乳腺癌恶性进展信号机制的认识，为探寻基于GPR30信号通路的乳腺癌治疗新策略提供实验依据。

Estrogen is the primary sex hormone in women，playing a key role in regulation of the growth/development and physiological function of the female reproductive system and breasts, under abnormal conditions, however, it exerts important effects on the malignant progression of breast cancer. The novel estrogen receptor, G protein-coupled receptor 30 (GPR30), has been found to be closely associated with invasion and metastasis in breast cancer，yet its signaling mechanism(s) remains unclear.We here tried to hypothesize that there may be a GPR30-calpain-FAK（focal adhesion kinase) pathway that promotes invasion and metastasis in breast cancer.In this project, we will set out to assess how GPR30 regulates the calpain system and whether there is a positive loop between calpain and FAK so as to understand the regulation of the GPR30-calpain-FAK signaling, and investigate its role in malignant biological behaviors such as migration, invasion, anti-anoikis and anchorage-independet growth at cellular and molecular levels.And xenograft in nude mice will be used to validate the results from the in vitro studies,hoping to find a key molecule(s) involved in controlling metastasis of breast cancer，and deepen our understanding of the signaling mechanism(s)that underlies the vicious development of berast cancer,providing experimental evidence to explore a novel strategy for the treatment of breast cancer.