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SET癌蛋白的过表达与人类胃癌的肿瘤进展及不良预后相关。

Overexpression of SET oncoprotein is associated with tumor progression and poor prognosis in human gastric cancer.

作者信息

Yuan Xiaoning, Zhang Te, Zheng Xin, Zhang Yunfei, Feng Tingting, Liu Pengfei, Sun Zhiting, Qin Shanshan, Liu Xuewen, Zhang Liang, Song Jie, Liu Ying

机构信息

Laboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan, Hubei 442000, P.R. China.

Department of Gastrointestinal Surgery, Dongfeng General Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, P.R. China.

出版信息

Oncol Rep. 2017 Sep;38(3):1733-1741. doi: 10.3892/or.2017.5788. Epub 2017 Jul 4.

Abstract

SE translocation (SET) oncoprotein, an inhibitor of protein phosphatase 2A, is abnormally expressed in many cancers. In this study, SET was aberrantly upregulated in gastric cancer (GC) compared with control tissues. Clinicopathological analysis showed that SET expression was significantly correlated with pathological grade (p=0.002), lymph node stage (p=0.014), and invasive depth (p=0.022). Kaplan-Meier analysis indicated that patients with high SET expression showed poorer overall survival rates than those with low SET expression. Moreover, SET knockdown downregulated GC cell proliferation, colony formation, tumorigenesis, and metastasis. The biological effect of SET on proliferation and invasion was mediated by inhibition of protein phosphatase 2, which in turn, activated Akt. Taken together, our results suggested that SET overexpression is associated with GC progression, and it might be a potential diagnostic marker for GC, thereby a possible target for GC drug development.

摘要

SET易位(SET)癌蛋白是蛋白磷酸酶2A的一种抑制剂,在许多癌症中异常表达。在本研究中,与对照组织相比,SET在胃癌(GC)中异常上调。临床病理分析表明,SET表达与病理分级(p = 0.002)、淋巴结分期(p = 0.014)和浸润深度(p = 0.022)显著相关。Kaplan-Meier分析表明,SET高表达患者的总生存率低于SET低表达患者。此外,SET基因敲低下调了GC细胞的增殖、集落形成、肿瘤发生和转移。SET对增殖和侵袭的生物学效应是通过抑制蛋白磷酸酶2介导的,进而激活Akt。综上所述,我们的结果表明SET过表达与GC进展相关,它可能是GC的一个潜在诊断标志物,从而可能是GC药物开发的一个靶点。

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