Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS.
Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS.
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DOI：
10.18632/oncotarget.9454
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发表时间：
2016-06-14
期刊：
影响因子：
--
通讯作者：
Zhang Z
中科院分区：
文献类型：
--
作者：
He F;Wei L;Luo W;Liao Z;Li B;Zhou X;Xiao X;You J;Chen Y;Zheng S;Li P;Murata M;Huang G;Zhang Z
谷氧还蛋白3（Glutaredoxin 3，GLRX 3）是一种抗氧化酶，维持低水平的ROS，从而有助于几种类型的癌症的生存和转移。然而，GLRX 3在鼻咽癌（NPC）中的表达和功能尚未得到解决。在本研究中，我们发现GLRX 3在NPC中过表达。在NPC细胞系中敲低GLRX 3抑制体外增殖、体内致瘤和集落形成。此外，GLRX 3基因敲低通过逆转上皮-间质转化（EMT）降低NPC细胞的迁移和侵袭能力。此外，GLRX 3的稳定性与表皮生长因子受体（EGFR）的表达呈正相关，与ROS的产生呈负相关。Akt的磷酸化，一个关键的下游效应，诱导EGFR信号，但不依赖于增加ROS水平在NPC细胞。GLRX 3可能是NPC中的一种癌蛋白，在增强氧化还原反应和激活EGFR/ Akt信号中起重要作用，因此有可能成为NPC治疗的靶点。
Glutaredoxin 3 (GLRX3) is antioxidant enzyme, maintaining a low level of ROS, thus contributing to the survival and metastasis of several types of cancer. However, the expression and functions of GLRX3 have not been addressed in nasopharyngeal carcinoma (NPC). In this study, we found that GLRX3 was overexpressed in NPC. Knockdown of GLRX3 in NPC cell lines inhibited proliferation in vitro, tumorignesis in vivo, and colony formation. In addition, GLRX3 knockdown decreased the migration and invasion capacity of NPC cells by reversing the epithelial-mesenchymal transition (EMT). Furthermore, stabilization of GLRX3 was positively related to with epidermal growth factor receptor (EGFR) expression and negatively with ROS generation. Phosphorylation of Akt, a key downstream effector, was induced by EGFR signaling but did not rely on increasing ROS level in NPC cells. GLRX3 might be an oncoprotein in NPC, playing important roles in increasing redox reaction and activating EGFR/ Akt signals, so it may be a therapeutic target for NPC.
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