Enolase-phosphatase 1 as a novel potential malignant glioma indicator promotes cell proliferation and migration
Enolase-phosphatase 1 as a novel potential malignant glioma indicator promotes cell proliferation and migration
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烯醇化磷酸酶1作为一种新型潜在恶性胶质瘤指标促进细胞增殖和迁移
DOI：
10.3892/or.2018.6592
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发表时间：
2018-10-01
期刊：
影响因子：
4.2
通讯作者：
Xu, Guozheng
中科院分区：
文献类型：
--
作者：
Su, Li;Yang, Ke;Xu, Guozheng
烯醇化磷酸酶 1 (ENOPH1) 是一种参与多胺生物合成并与应激反应相关的酶。然而，人们对其在神经胶质瘤病理生理学中的作用知之甚少。在本研究中，我们检测了 ENOPH1 在人胶质瘤组织和细胞系中的表达和功能。采用Western blot、qPCR和免疫组化分析86例患者胶质瘤组织中ENOPH1蛋白的表达情况。采用 3-[4,5-二甲基噻唑-2-基]-2,5-二苯基溴化四唑 (MTT)、伤口愈合和细胞周期测定来鉴定 U87 和 U251 神经胶质瘤细胞中的细胞生长和细胞迁移。结果显示，与正常脑组织相比，胶质瘤组织中ENOPH1的水平显着升高。此外，我们观察到胶质瘤病理分级与ENOPH1的表达水平呈正相关。用 siRNA 敲低 ENOPH1 表达可显着降低细胞增殖，并显着降低细胞迁移。值得注意的是，ENOPH1的敲低促进其下游蛋白酸还原酮双加氧酶1（ADI1）从U251胶质瘤细胞的细胞核转移到细胞质，而MT1-MMP表达与对照组相比显着下调。总的来说，我们的数据表明，ENOPH1 的敲低抑制了细胞生长和迁移，这可能与胶质瘤细胞中 ADI1 易位和 MT1-MMP 下调有关。因此，ENOPH1可以作为神经胶质瘤的潜在治疗靶点。
Enolase-phosphatase 1 (ENOPH1), is an enzyme that is involved in polyamine biosynthesis and is associated with stress responses. However, little is known about its role in the pathophysiology of glioma. In the present study, we examined the expression and function of ENOPH1 in human glioma tissues and cell lines. Western blot, qPCR and immunohistochemistry analysis were performed to investigate the expression of the ENOPH1 protein in glioma tissues in 86 patients. The 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT), wound healing and cell cycle assays were implemented to identify cell growth and cell migration in U87 and U251 glioma cells. The results revealed that compared with normal brain tissues, the level of ENOPH1 was markedly increased in glioma tissues. In addition, we observed that the glioma pathological grade was positively associated with the expression level of ENOPH1. Knockdown of ENOPH1 expression with siRNA markedly reduced cell proliferation, and significantly decreased cell migration. Notably, knockdown of ENOPH1 promoted its downstream protein, aci-reductone dioxygenase 1 (ADI1), to shift from the nucleus to the cytoplasm of U251 glioma cells, while MT1-MMP expression was significantly downregulated compared with the control group. Collectively, our data demonstrated that the knockdown of ENOPH1 suppressed cell growth and migration, which may be associated with ADI1 translocation and MT1-MMP downregulation in glioma cells. Thus, ENOPH1 could serve as an underlying therapeutic target of glioma.