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首页> 美国卫生研究院文献>Cancer Medicine >HIF‐1α binding to AEG‐1 promoter induced upregulated AEG‐1 expression associated with metastasis in ovarian cancer
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HIF‐1α binding to AEG‐1 promoter induced upregulated AEG‐1 expression associated with metastasis in ovarian cancer

机译：HIF-1α与AEG-1启动子的结合诱导卵巢癌转移相关的AEG-1表达上调

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Ovarian cancer with the highest mortality rate among gynecological malignancies is one of common cancers among female cancer patients. As reported in recent years, AEG‐1 was associated with the occurrence, development, and metastasis of ovarian cancer, but the mechanisms remain unclear. In the current study, invasion capabilities of ovarian cancer OVCAR3 cells were measured by viral infection and transwell assay. Western blot analysis was used to evaluate the expression levels of β‐catenin, E‐cadherin, MMP2, and MMP9. With qRT‐PCR analysis, AEG‐1 and HIF‐1α gene expression were detected. We used luciferase reporter gene to measure AEG‐1 promoter activity under normoxia/hypoxia in OVCAR3 cells. Our work demonstrated that AEG‐1 significantly enhanced invasion capabilities of OVCAR3 cells and the expression levels of β‐catenin, E‐cadherin, MMP2, and MMP9 associated with invasion capabilities of OVCAR3 cells were upregulated. Furthermore, hypoxia enhanced invasion capabilities of OVCAR3 cells and induced style="fixed-case">AEG‐1 high gene expression, which was reversed by style="fixed-case">AEG‐1 knockdown lentivirus. style="fixed-case">HIF‐1α expression upregulation was induced in style="fixed-case">OVCAR3 cells after hypoxia. style="fixed-case">HIF‐1α knockdown lentivirus induced downregulated expression of style="fixed-case">AEG‐1 and invasion capabilities of style="fixed-case">OVCAR3 cells were also inhibited. Wild‐type style="fixed-case">AEG‐1 promoter activity under hypoxic conditions was significantly higher than that AEG‐1 mutation under normoxic conditions in the absence of hypoxia response. Our results suggested that style="fixed-case">HIF‐1α binds to style="fixed-case">AEG‐1 promoter to upregulate its expression, which was correlated with metastasis in ovarian cancer by inducing the expression of style="fixed-case">MMP2 and style="fixed-case">MMP9 as well as inhibiting expression of E‐cadherin and β‐catenin.
机译：在妇科恶性肿瘤中死亡率最高的卵巢癌是女性癌症患者中的常见癌症之一。如近年来报道，AEG-1与卵巢癌的发生，发展和转移有关，但机制尚不清楚。在当前的研究中，通过病毒感染和transwell测定法测定了卵巢癌OVCAR3细胞的侵袭能力。 Western blot分析用于评估β-catenin，E-cadherin，MMP2和MMP9的表达水平。通过qRT-PCR分析，检测到AEG-1和HIF-1α基因表达。我们使用萤光素酶报告基因来测量OVCAR3细胞在常氧/低氧下的AEG-1启动子活性。我们的工作表明，AEG-1显着增强了OVCAR3细胞的侵袭能力，并且与OVCAR3细胞侵袭能力相关的β-catenin，E-cadherin，MMP2和MMP9的表达水平被上调。此外，低氧增强了OVCAR3细胞的侵袭能力并诱导了 style =“ fixed-case”> AEG -1高基因表达，而 style =“ fixed-case”> AEG ‐1敲低慢病毒。缺氧后， style =“ fixed-case”> HIF -1α表达在 style =“ fixed-case”> OVCAR 3细胞中被诱导上调。 style =“ fixed-case”> HIF ‐1α敲低慢病毒诱导 style =“ fixed-case”> AEG -1的表达下调和 style =“ fixed的入侵能力-case“> OVCAR 3细胞也被抑制。在缺氧条件下，缺氧条件下的野生型 style =“ fixed-case”> AEG -1启动子活性明显高于在常氧条件下的AEG-1突变。我们的结果表明， style =“ fixed-case”> HIF -1αα与 style =“ fixed-case”> AEG -1启动子结合以上调其表达，这与诱导 style =“ fixed-case”> MMP 2和 style =“ fixed-case”> MMP 9的表达并抑制E‐钙粘蛋白和β-连环蛋白。

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