Abstract：
Cell cycle dysregulation leading to uncontrolled growth is a primary characteristic of malignancy. GSG2, a mitosis-related kinase, affects the normal cell cycle by interfering with the normal dissociation of centromere cohesion, and its overexpression has been shown to play an important role in cancer cells. Here, we investigated the function of GSG2 as a tumor promoter in endometrial carcinoma and its relationship with the immunological microenvironment. We used immunohistochemistry to identify a correlation between the development and prognosis of GSG2 and endometrial cancer. Cell and animal experiments confirmed that GSG2 has a protumorigenic phenotype in endometrial cancer cell lines. Furthermore, using GeneChip analysis and a tumor-immune coculture model, we observed a link between GSG2 expression and the composition of the immune microenvironment. Therefore, we concluded that the activation of the PI3K/AKT pathway by GSG2 may impact DNA repair, disrupt the cell cycle, and regulate the immune response, all of which could increase the ability of EC cells to proliferate malignantly. Consequently, it is anticipated that GSG2 will be a viable therapeutic target in endometrial carcinoma.
摘要：
导致不受控制的生长的细胞周期失调是恶性肿瘤的主要特征。GSG2，一种有丝分裂相关激酶，通过干扰着丝粒内聚力的正常解离来影响正常的细胞周期，并且其过度表达已被证明在癌细胞中起重要作用。这里,我们研究了GSG2在子宫内膜癌中作为肿瘤启动子的功能及其与免疫微环境的关系。我们使用免疫组织化学来确定GSG2的发展和预后与子宫内膜癌之间的相关性。细胞和动物实验证实GSG2在子宫内膜癌细胞系中具有原瘤表型。此外，使用基因芯片分析和肿瘤免疫共培养模型，我们观察到GSG2表达与免疫微环境组成之间存在联系。因此,我们得出结论，GSG2激活PI3K/AKT通路可能会影响DNA修复，破坏细胞周期,调节免疫反应，所有这些都可以增加EC细胞的恶性增殖能力。因此,预计GSG2将是子宫内膜癌的可行治疗靶标.
