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真核生物翻译起始因子3亚基G促进人类结直肠癌。

Eukaryotic translation initiation factor 3 subunit G promotes human colorectal cancer.

作者信息

Yang Chenggang, Zhang Yanbo, Du Wenfeng, Cheng Honggang, Li Chaobin

机构信息

Department of Gastrointestinal Surgery, Liaocheng People's Hospital Liaocheng 252000, Shandong, China.

出版信息

Am J Transl Res. 2019 Feb 15;11(2):612-623. eCollection 2019.

PMID:30899366
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6413245/
Abstract

In this study, we investigated the role of eukaryotic translation initiation factor 3 subunit G (EIF3G) in colorectal cancer. Immunohistochemical analysis showed higher EIF3G expression in stage IV human colorectal cancer tissues than in adjacent normal tissues (P<0.01). EIF3G short hairpin RNA (shRNA) knockdown in HCT116 colon cancer cells reduced proliferation and increased apoptosis as compared to control. EIF3G knockdown also increased autophagy and reduced mTOR signaling, as evidenced by low phospho-AKT, phospho-S6K and phospho-4EBP1 levels. Functional experiments indicated that overexpression of EIF3G promoted HCT-116 cells proliferation, migration and xenograft tumor growth. Finally, we observed lower xenograft tumor weights and volumes with EIF3G-silenced HCT116 cells than with control cells. These findings demonstrate that EIF3G promotes colon cancer growth and is a potential therapeutic target.

摘要

在本研究中,我们调查了真核生物翻译起始因子3亚基G(EIF3G)在结直肠癌中的作用。免疫组织化学分析显示,IV期人类结直肠癌组织中EIF3G的表达高于相邻正常组织(P<0.01)。与对照组相比,HCT116结肠癌细胞中EIF3G短发夹RNA(shRNA)敲低可降低细胞增殖并增加细胞凋亡。EIF3G敲低还增加了自噬并降低了mTOR信号传导,低磷酸化AKT、磷酸化S6K和磷酸化4EBP1水平证明了这一点。功能实验表明,EIF3G的过表达促进了HCT-116细胞的增殖、迁移和异种移植肿瘤生长。最后,我们观察到,与对照细胞相比,EIF3G沉默的HCT116细胞的异种移植肿瘤重量和体积更低。这些发现表明,EIF3G促进结肠癌生长,是一个潜在的治疗靶点。

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