EYA4通过下调胶质瘤中的p27Kip1促进细胞增殖。
EYA4 Promotes Cell Proliferation Through Downregulation of p27Kip1 in Glioma.
作者信息
Li Zhaoming, Qiu Ran, Qiu Xia, Tian Tian
机构信息
Department of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Wuhan Institute of Bioengineering, Wuhan, China.
出版信息
Cell Physiol Biochem. 2018;49(5):1856-1869. doi: 10.1159/000493631. Epub 2018 Sep 19.
BACKGROUND/AIMS: Accumulating evidence suggests that Eyes Absent Homologue 4 (EYA4) plays an important role in tumorigenesis and progression of various cancers. However, the role of EYA4 in glioma development is still unclear.
METHODS
The expression of EYA4 was examined in glioma tissues by immunohistochemistry. Cell viability and apoptosis were analyzed by CCK-8, BrdU assay, and flow cytometry.
RESULTS
We found that EYA4 was upregulated in glioma, and its expression was positively correlated with advanced tumor stage. Moreover, higher expression of EYA4 predicted a worse overall survival in patients with glioma. Forced overexpression of EYA4 enhanced glioma cell proliferation, and EYA4 suppressed the expression of p27Kip1 directly in these cells. Furthermore, Six1 was required for EYA4 to suppress the expression of p27Kip1 in glioma.
CONCLUSION
Together, we demonstrate that EYA4 promotes cell proliferation by directly suppressing the expression of p27Kip1 in glioma.
背景/目的：越来越多的证据表明，无眼同源物4（EYA4）在多种癌症的发生和发展中起重要作用。然而，EYA4在胶质瘤发生中的作用仍不清楚。
方法
采用免疫组织化学法检测胶质瘤组织中EYA4的表达。通过CCK-8、BrdU检测和流式细胞术分析细胞活力和凋亡情况。
结果
我们发现EYA4在胶质瘤中上调，其表达与肿瘤晚期呈正相关。此外，EYA4的高表达预示着胶质瘤患者的总生存期较差。EYA4的强制过表达增强了胶质瘤细胞的增殖，并且EYA4直接抑制了这些细胞中p27Kip1的表达。此外，Six1是EYA4在胶质瘤中抑制p27Kip1表达所必需的。
结论
我们共同证明，EYA4通过直接抑制胶质瘤中p27Kip1的表达来促进细胞增殖。
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