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过表达的 DNA 结合蛋白抑制剂 2 作为一个不利的预后因素促进鼻咽癌的细胞增殖。

Overexpressed DNA-binding protein inhibitor 2 as an unfavorable prognosis factor promotes cell proliferation in nasopharyngeal carcinoma.

机构信息

Department of Pathology, Basic School of Guangzhou Medical College, Guangzhou 510182, China.

出版信息

Acta Biochim Biophys Sin (Shanghai). 2012 Jun;44(6):503-12. doi: 10.1093/abbs/gms030. Epub 2012 May 2.

DOI:10.1093/abbs/gms030
PMID:22551584
Abstract

The aim of the present study was to analyze the expression of DNA-binding protein inhibitor 2 (ID2) in nasopharyngeal carcinoma (NPC) and its correlation with clinicopathological features. It was found that the expression of ID2 was significantly increased in NPC cells when compared with that in NP69 cell line. Similar level of ID2 cytoplasmic expression was observed in NPC when compared with that in non-cancerous nasopharynx tissues. However, the level of ID2 in nucleus was increased in NPC when compared with that in normal nasopharynx tissues. Furthermore, the higher expression level of nuclear ID2 was significantly associated with tumor size (T classification), lymph node metastasis (N classification), and clinical stage. Patients with increased ID2 expression level had poorer overall survival rates than those with low ID2 levels. The inhibition of ID2 expression in NPC cell line SUNE1 by lentiviral-mediated short hairpin RNA could suppress cell proliferation and colony formation, but did not disrupt cell migration. Knocking down the expression of ID2 by RNA interference could down-regulate the expression of Snail, suggesting that ID2-promoted cell growth, partially attributing to the regulation of Snail activity in NPC. Our study demonstrated that over-expression of ID2 protein is an unfavorable prognostic factor which promotes cell proliferation in NPC.

摘要

本研究旨在分析 DNA 结合蛋白抑制剂 2(ID2)在鼻咽癌(NPC)中的表达及其与临床病理特征的相关性。结果发现,与 NP69 细胞系相比,ID2 在 NPC 细胞中的表达显著增加。与非癌性鼻咽组织相比,NPC 中 ID2 的细胞质表达水平相似。然而,与正常鼻咽组织相比,NPC 中 ID2 的核内水平增加。此外,核内 ID2 表达水平越高,与肿瘤大小(T 分类)、淋巴结转移(N 分类)和临床分期的相关性越显著。ID2 表达水平升高的患者总生存率明显低于 ID2 水平较低的患者。通过慢病毒介导的短发夹 RNA 抑制 NPC 细胞系 SUNE1 中的 ID2 表达可抑制细胞增殖和集落形成,但不破坏细胞迁移。通过 RNA 干扰敲低 ID2 的表达可下调 Snail 的表达,提示 ID2 促进 NPC 中的细胞生长部分归因于对 Snail 活性的调节。本研究表明,ID2 蛋白的过表达是一个不利的预后因素,可促进 NPC 中的细胞增殖。

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