Golgi Phosphoprotein 3 Inhibits the Apoptosis of Human Glioma Cells in Part by Downregulating N-myc Downstream Regulated Gene 1.

Golgi Phosphoprotein 3 Inhibits the Apoptosis of Human Glioma Cells in Part by Downregulating N-myc Downstream Regulated Gene 1.
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高尔基磷蛋白 3 部分通过下调 N-myc 下游调节基因 1 抑制人胶质瘤细胞凋亡

DOI:
10.12659/msm.900349
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发表时间:
2016-10-04
期刊:
Medical science monitor : international medical journal of experimental and clinical research
影响因子:
--
通讯作者:
Li X
Li X
中科院分区:
其他
文献类型:
--
作者:
Li X;Li M;Tian X;Li Q;Lu Q;Jia Q;Zhang L;Yan J;Li X;Li X

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据报道,高尔基磷酸化蛋白3 (GOLPH3)参与了几种人类癌症的发展。我们前期的研究表明GOLPH3在胶质瘤组织中的表达与肿瘤的恶性程度有关。然而,GOLPH3影响细胞凋亡的机制在很大程度上是未知的。本研究旨在探讨GOLPH3参与细胞凋亡的可能机制。材料/方法利用GOLPH3小干扰RNA介导胶质瘤细胞凋亡,分析GOLPH3在胶质瘤细胞中的生物学作用。流式细胞术检测胶质瘤细胞凋亡。分别通过Western blot和免疫组化染色检测GOLPH3和NDRG1蛋白的表达水平,以评价其与胶质瘤的关系。采集胶质瘤患者的肿瘤组织。正常脑组织来自于接受内减压手术的脑外伤患者。结果证实GOLPH3的降低促进胶质瘤细胞的凋亡可能受NDRG1和cleaved capcase 3的激活调控。胶质瘤样品中GOLPH3和NDRG1呈负相关。结论GOLPH3和NDRG1在胶质瘤发病中均起重要作用。GOLPH3或NDRG1可能是恶性胶质瘤治疗的潜在候选者。
Background Golgi phosphoprotein 3 (GOLPH3) has been reported to be involved in the development of several human cancers. Our previous study showed that GOLPH3 expression in glioma tissues was related to the severity of the malignancy of the cancer. However, the mechanism by which GOLPH3 affects cell apoptosis is largely unknown. The present study was designed to explore the possible mechanism of GOLPH3 in cell apoptosis. Material/Methods To analyze the biological role of GOLPH3 in glioma cells, we used GOLPH3 small interference RNA in apoptosis of glioma cells. The apoptosis of glioma cells was detected by flow cytometry. The expression level of GOLPH3 and NDRG1 protein was determined by Western blot analyses and immunohistochemical staining, respectively, to evaluate their association with glioma. Tumor tissues were collected from patients with glioma. Normal cerebral tissues were acquired from cerebral trauma patients undergoing internal decompression surgery. Results We confirm that the decrease of GOLPH3 that promotes the apoptosis of glioma cells may be regulated by the activation of NDRG1 and cleaved capcase 3. There was a inverse association between GOLPH3 and NDRG1 in glioma samples. Conclusions Our findings indicate that GOLPH3 and NDRG1 both play an important role in glioma etiology. Either GOLPH3 or NDRG1 might be a potential candidate for malignant glioma therapy.
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