Overexpression of Peroxiredoxin 6 (PRDX6) Promotes the Aggressive Phenotypes of Esophageal Squamous Cell Carcinoma.
Overexpression of Peroxiredoxin 6 (PRDX6) Promotes the Aggressive Phenotypes of Esophageal Squamous Cell Carcinoma.
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过氧化还原蛋白 6 (PRDX6) 的过度表达促进食管鳞状细胞癌的侵袭性表型。
DOI：
10.7150/jca.26041
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发表时间：
2018
影响因子：
3.9
通讯作者：
Cao J
中科院分区：
文献类型：
--
作者：
He Y;Xu W;Xiao Y;Pan L;Chen G;Tang Y;Zhou J;Wu J;Zhu W;Zhang S;Cao J
食管鳞状细胞癌（ESCC）是最常见的恶性肿瘤之一。过氧化还原蛋白6（PRDX6）是过氧化物酶超家族的成员，具有消除活性氧（ROS）的功能，参与包括肿瘤在内的多种疾病的发生发展。本研究的目的是调查 PRDX6 在正常和癌性食管组织中的表达，并表征其在 ESCC 进展中的作用。我们发现食管鳞癌组织中 PRDX6 的表达量显着高于正常食管组织或癌旁组织，且 PRDX6 表达水平与增殖相关标志物呈正相关。在 ESCC 细胞中，PRDX6 分布在细胞核区域更为明显。腺病毒过表达 PRDX6 显着促进 TE-1 和 Eca-109 细胞的增殖、迁移和侵袭。相反，慢病毒介导的 PRDX6 表达敲低显着减少了 ESCC 细胞的细胞生长、集落形成和转移。 PRDX6 调节 Akt 和 Erk1/2 的磷酸化以及 MMP2 的表达。我们还发现 PRDX6 和 Erk1/2 通路在 ESCC 细胞中相互调节。此外，PRDX6 过表达消除了辐射诱导的 ROS，并减少了随后的细胞凋亡，表明其在放射抗性中发挥作用。最后，PRDX6促进肿瘤生长的作用在ESCC异种移植裸鼠中得到进一步证实。综上所述，我们证明PRDX6的过度表达通过Erk1/2促进ESCC的进展，这为人类ESCC提供了潜在的治疗靶点。
Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies. Peroxiredoxin 6 (PRDX6), a member of peroxidase superfamily, has a function of eliminating the reactive oxygen species (ROS), and participates in development of multiple diseases, including tumors. The purpose of this study was to investigate the expression of PRDX6 in normal and cancerous esophageal tissues and to characterize its role in ESCC progression. We found significantly higher expression of PRDX6 in ESCC tissues than in normal esophageal tissues or tumor-adjacent tissues and that the PRDX6 expression level was positively correlated with the proliferation-related markers. In ESCC cells, PRDX6 distribution was more pronounced in the nucleus region. PRDX6 overexpression by an adenovirus significantly promoted cell proliferation, migration and invasion in TE-1 and Eca-109 cells. Conversely, lentivirus-mediated knock-down of PRDX6 expression significantly reduced cell growth, colony formation and metastasis in ESCC cells. PRDX6 modulated the phosphorylation of Akt and Erk1/2, and the expression of MMP2. We also found that PRDX6 and Erk1/2 pathway were mutually regulated in ESCC cells. In addition, PRDX6 overexpression eliminated radiation-induced ROS and decreased consequent cell apoptosis, indicative of a role in radioresistance. Finally, the role of PRDX6 in promoting tumor growth was further confirmed in nude mice with ESCC xenografts. Taken together, we demonstrated that overexpression of PRDX6 promotes the progression of ESCC through Erk1/2, which provides a potential therapeutic target for human ESCC.
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DOI：
10.1186/bcr1789
发表时间：
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期刊：
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影响因子：
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