子宫内膜癌中PI3K/AKT及JAK/STAT信号通路与IDO介导的免疫逃逸机制研究进展

Advances in relationships of PI3K/AKT and JAK/STAT signaling pathways and the immune escape mechanisms mediated by IDO in endomrtial cancer

子宫内膜癌是女性生殖系统中最常见的一种恶性肿瘤,其发生和发展与多条信号通路的异常以及肿瘤相关基因的突变有关。磷脂肌醇3-激酶(phosphoinositide-3kinase,PI3K)-蛋白激酶B(protein kinase B,PKB,又称AKT)信号通路与Janus激酶(janus kinase,JAK)/信号转导及转录激活因子(signal transducer andactivator of transcription,STAT)信号通路是近几年来与子宫内膜癌发生相关信号通路研究的热点;大量的研究发现,它们的调节异常与子宫内膜的发生、发展、预后以及复发密切相关。除了肿瘤相关基因异常外,有研究认为肿瘤的发生不仅是异常细胞以及恶性克隆的产生,还与肿瘤的免疫逃逸(tumor immune escape)有关,其可使机体不能及时的清除异常组织,从而介导了肿瘤的发生、侵袭与转移。有研究发现,在肿瘤免疫逃逸过程中发挥重要作用的吲哚胺2,3双加氧酶(indoleamine2,3-dioxygenase,IDO)与上述两条通路存在密切的关联,这可能正是肿瘤组织在机体中不仅能够稳定繁殖,还不易被机体免疫系统清除的关键所在。因此,本文旨在就上述两条信号通路与IDO相关性的研究作一综述。

Endometrial cancer is one of the most common vaginal cancers in females. The dysregulation of numerous signaling pathways and tumor-related genes have been reported to play important roles in the progression of endometrial cancer. Recently, PI3K （phosphoinositide 3-kinase）/AKT （protein kinase B） and JAK （Janus kinase）/STAT （signal transducer and activator of transcription） signaling pathways have been the focus of study. A large number of studies have identified the role of these two signaling pathways in the regulation of tumorigenesis, progression and prognosis of endometrial cancer. Some studies have suggested that immune escape may play an important role in the tumorigenesis and progression of endometrial cancer. IDO （indoleamine 2, 3-dioxygenase） which has been demontrated to play an important role in immune escape of tumor, was reported to be associated with these two signaling pathways. This may be the key reason for tumor escaping from immune recognition. This review focuses on the relationship of PI3K/AKT and JAK/STAT signaling pathways and IDO, aiming to explain the mechanism of tumorigenesis and progression of endometrial cancer.