卵巢癌的复发转移是导致患者死亡的主要原因，因此研究其可能机制是目前临床亟待解决的重大问题。本课题组前期研究发现雌激素剌激体外培养的EOC细胞株可使其增殖和侵袭能力增强，但其具体机制仍不清楚。随后采用基因芯片筛查雌激素刺激EOC细胞后TRPC3转录水平升高。随着对肿瘤侵袭转移研究的深入，我们首次提出雌激素可能通过结合雌激素受体，上调了卵巢癌细胞上的TRPC3受体，而增多的TRPC3介导SOCE过程，从而导致肿瘤细胞内Ca2+升高，并调控了卵巢癌的发生发展及侵袭转移过程，这对于卵巢癌的研究无疑是全新的认识。本课题拟借助分子生物学等技术深入研究雌激素通过TRPC3发挥促进EOC侵袭转移相关的生物学过程，丰富EOC发生与发展的雌激素相关假说，并为基于TRPC3相关的靶向治疗EOC提供一定的理论依据，进一步使我们从多层面多角度理解上皮性卵巢癌发生侵袭和转移的机制，为卵巢癌的治疗提供新的思路。

The major cause of death in ovarian cancer patients is metastasis and recurrence. The clinical major problems to be solved is the study of the molecular mechanisms of invasion and metastasis in ovarian cancer.Our previous studies have found that estrogen stimulation the EOC cells can make its enhancement in proliferation and invasive ability.But the mechanism remains unclear. Then the gene chip screening the effects on estrogen stimulation EOC cell lines, observed that level of TRPC3 transcription is increased. With the further research on tumor invasion and metastasis, We bring forward the hypothesis that estrogen may combine with estrogen receptor, increased TRPC3 on ovarian cancer cells, and increased TRPC3 mediated SOCE process, resulting in Ca2 + increases in tumor cells, and regulate the development of invasion and metastasis process in ovarian cancer.We are going to study on the estrogen promote the invasion and metastasis of EOC relevant biological processes by TRPC3 using molecular biology and other technologies, explore known and unknown pathway of the invasion and metastasis in ovarian cancer, and clarify the mechanism of the invasion and metastasis from the molecular level.