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锌指蛋白692(ZNF692)促进肺腺癌的增殖和细胞迁移。

ZNF692 promotes proliferation and cell mobility in lung adenocarcinoma.

作者信息

Zhang Quanli, Zheng Xiufen, Sun Qi, Shi Run, Wang Jie, Zhu Biqing, Xu Lin, Zhang Guangqin, Ren Binhui

机构信息

Department of Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, PR China; Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Nanjing, 210009, PR China; Department of Thoracic Surgery, Jiangsu Cancer Hospital, Institute Affiliated to Nanjing Medical University, Cancer Institute of Jiangsu Province, Baiziting 42, Xuanwu District, Nanjing, 210009, PR China.

Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Nanjing, 210009, PR China.

出版信息

Biochem Biophys Res Commun. 2017 Sep 2;490(4):1189-1196. doi: 10.1016/j.bbrc.2017.06.180. Epub 2017 Jun 29.

DOI:10.1016/j.bbrc.2017.06.180
PMID:28669730
Abstract

By analyzing The Cancer Genome Atlas (TCGA) datasets, we discovered that the zinc finger protein 692 (ZNF692) were over-expressed in Lung adenocarcinoma (LUAD) tissues compared to adjacent non-tumor tissues (P < 0.0001). In this study, we investigated the function of ZNF692 in the progression of LUAD. We found that ZNF692 knockdown inhibited LUAD cells proliferation, migration, and invasion both in vitro and in vivo. And LUAD cell apoptosis was induced following the down-regulation of ZNF692. Our results show that ZNF692 is over-expressed in LUAD tissues compared to adjacent normal tissues, and hyper-expression of ZNF692 in LUAD is an independent risk factor for worse overall survival in LUAD patients (HR: 8.800, 95%CI: 1.082-71.560, P = 0.042) by Tissue Microarray stain assay (TMA). GO analysis indicated that most genes were enriched in metabolic process which were associated highly with ZNF692 levels. Collectively, our results suggested that ZNF692 may serve as a potential oncogene and biomarker in LUAD by influencing cell metabolism.

摘要

通过分析癌症基因组图谱(TCGA)数据集,我们发现与相邻的非肿瘤组织相比,锌指蛋白692(ZNF692)在肺腺癌(LUAD)组织中过表达(P < 0.0001)。在本研究中,我们调查了ZNF692在LUAD进展中的功能。我们发现,ZNF692基因敲低在体外和体内均抑制LUAD细胞的增殖、迁移和侵袭。并且ZNF692下调后诱导了LUAD细胞凋亡。我们的结果表明,与相邻正常组织相比,ZNF692在LUAD组织中过表达,并且通过组织芯片染色分析(TMA),LUAD中ZNF692的高表达是LUAD患者总体生存较差的独立危险因素(HR:8.800,95%CI:1.082 - 71.560,P = 0.042)。基因本体(GO)分析表明,大多数基因富集在与ZNF692水平高度相关的代谢过程中。总体而言,我们的结果表明,ZNF692可能通过影响细胞代谢而成为LUAD中的潜在癌基因和生物标志物。

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引用本文的文献

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Discov Oncol. 2024 May 12;15(1):158. doi: 10.1007/s12672-024-01005-0.
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ZNF692 promotes osteosarcoma cell proliferation, migration, and invasion through TNK2-mediated activation of the MEK/ERK pathway.锌指蛋白 692 通过 TNK2 介导的 MEK/ERK 通路激活促进骨肉瘤细胞的增殖、迁移和侵袭。
Biol Direct. 2024 Apr 22;19(1):28. doi: 10.1186/s13062-024-00472-3.
3
ZNF692 drives malignant development of hepatocellular carcinoma cells by promoting ALDOA-dependent glycolysis.
ZNF692 通过促进 ALDOA 依赖性糖酵解驱动肝癌细胞的恶性发展。
Funct Integr Genomics. 2024 Mar 8;24(2):53. doi: 10.1007/s10142-024-01326-x.
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ZNF692 promotes cell proliferation, invasion and migration of human prostate cancer cells by targeting the EMT signaling pathway.ZNF692 通过靶向 EMT 信号通路促进人前列腺癌细胞的增殖、侵袭和迁移。
Eur J Med Res. 2024 Jan 30;29(1):88. doi: 10.1186/s40001-024-01645-6.
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Comprehensive analysis of ZNF692 as a potential biomarker associated with immune infiltration in a pan cancer analysis and validation in hepatocellular carcinoma.全面分析 ZNF692 作为一种潜在的生物标志物与泛癌分析中的免疫浸润相关,并在肝细胞癌中进行验证。
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