氧化应激与卵巢癌发病机制相关性的研究进展

摘要

Ovarian cancer is a common gynecologic malignant tumor which possesses the highest mortality in China.The occurrence of ovarian cancer is promoted by the abnormal expressions of Nrf2、PKC、GRB7/ERK/FOXM1,and that is induced by the increased level of ROS produced from body''s oxidative stress.A possible cause of the ovarian cancer cell metastasis is the increased level of ROS,which directly or indirectly influences the mediation between HIF-1 and downstream signaling,affects epithelial-mesenchymal transition and vasculogenic mimicry,promotes tumor angiogenesis and metastasis eventually.In addition,ovarian cancer can lead to TAM infiltration and induce the high expression of regulatory signals,such as Notch in hypoxic microenvironment,which promote ovarian cancer stem cell self-renewal and strengthen the ability of invasion and metastasis of ovarian cancer.In recent years,the relationship between ovarian cancer and oxidative stress and the inhibition of cancer''s occurrence and development induced by anti-oxidative have been researched as a hot topic.This article reviews the research progress on the correlation between oxidative stress and the development,invasion and metastasis of ovarian cancer.%卵巢癌是我国常见的死亡率最高的妇科恶性肿瘤.机体内由氧化应激所产生的活性氧水平升高,介导Nrf2、PKC、GRB7/ERK/FOXM1异常表达,可促使卵巢癌的发生.同时卵巢癌细胞内活性氧水平升高可能是导致卵巢癌细胞转移的重要原因,通过直接或间接影响HIF-1介导下游信号从而引起上皮间充质转变和血管形成拟态,促进肿瘤血管形成,最终发生转移.另外,卵巢癌在缺氧的微环境下可使肿瘤相关巨噬细胞(tumor-associated marophages,TAM)浸润;并诱导卵巢癌干细胞高表达Notch等调节信号,促进卵巢癌干细胞自我更新,进一步加强卵巢癌的侵袭、转移能力.近年来,氧化应激与卵巢癌的关系以及通过抗氧化抑制其发生、发展已成为研究热点.本文就氧化应激机制与卵巢癌的发生发展及侵袭转移机制的相关性研究进展做一综述.