肿瘤细胞的高侵袭迁移能力是卵巢癌患者预后极差的重要原因。我们课题组在前期研究发现，dysbindin促进卵巢癌侵袭转移，但具体机制尚不明确。我们近期结果提示dysbindin可抑制PTEN磷酸化，增强PI3K/AKT-mTOR通路活性。同时，基于测序发现miR-551b-3p是受dysbindin调控的关键分子，而mTOR可负调控miR-551b-3p表达并与miR-551b-3p下游靶分子ZEB1共同在卵巢癌侵袭转移中发挥重要作用。上述结果高度提示dysbindin可能通过调控PTEN/miR-551b-3p/ZEB1通路促进卵巢癌侵袭转移。本课题拟进一步解析dysbindin调控这一通路的分子机制，明确dysbindin调控该通路促进卵巢癌侵袭转移的生物学功能，并揭示其临床意义，为卵巢癌的防治提供新的理论依据和潜在治疗靶点。

The high invasion and migration capacity of tumor cells is an important reason for the poor prognosis of patients with ovarian cancer. In our previous research, our research group found that dysbindin promotes ovarian cancer invasion and metastasis, but the specific mechanism is not clear. Pre-experiments suggest that dysbindin can negatively regulate PTEN phosphorylation and enhance PI3K/AKT-mTOR pathway activity. In addition, based on sequencing, miR-551b-3p was found to be a key molecule regulated by dysbindin, and mTOR can negatively regulate miR-551b-3p expression and play an important role in the invasion and metastasis of ovarian cancer together with ZEB1, a downstream target molecule of miR-551b-3p. The above results highly suggest that dysbindin may promote the invasion and metastasis of ovarian cancer through the PTEN/miR-551b-3p/ZEB1 pathway. Based on previous research and pre-experiments, this project intends to further analyze the molecular mechanism of dysbindin regulation of this pathway to clarify the biological function of dysbindin regulation of this pathway in promoting ovarian cancer invasion and metastasis, and to reveal its clinical significance, so as to provide a new potential therapeutic target for the prevention and treatment of ovarian cancer.