TRIM47 overexpression is a poor prognostic factor and contributes to carcinogenesis in non-small cell lung carcinoma

肺癌 肿瘤科 内科学 免疫组织化学 癌症 腺癌 生存分析 比例危险模型
作者
Yudong Han,Tian Haiying,Pei Chen,Qiang Lin
出处
期刊:Oncotarget [Impact Journals LLC]
卷期号:8 (14): 22730-22740 被引量:24
标识
DOI:10.18632/oncotarget.15188
摘要

// Yudong Han 1, * , Haiying Tian 2, * , Pei Chen 1 , Qiang Lin 1 1 Department of Thoracic Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China 2 Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China * These authors contributed equally to this work Correspondence to: Qiang Lin, email: xklinqiang@hotmail.com Keywords: TRIM47, NSCLC, cell cycle, P53, EMT Received: August 08, 2016      Accepted: January 23, 2017      Published: February 08, 2017 ABSTRACT Non-small cell lung carcinoma (NSCLC) is the most common malignancy with the highest morbidity and mortality. In this study, we found that tripartite motif containing 47 (TRIM47) expression level was higher in tumor tissues than in normal adjacent tissues. Overexpression of TRIM47 closely correlated with poor prognosis in patients with NSCLC. Multivariate Cox regression analyses showed that TRIM47 overexpression could be considered an independent prognostic factor for NSCLC. TRIM47 depletion significantly inhibited cell proliferation and induced G1phase arrest in A549 and H358 cell lines. Moreover, TRIM47 silencing remarkably inhibited cell migration, cell invasion, and tumorigenicity in nude mice. Gene set enrichment analysis (GSEA) revealed that cancer-related process and pathways, including p53-cell cycle and NFκB-epithelial mesenchymal transition (EMT) pathway, were significantly correlated with TRIM47 expression. Real-time PCR and Western blot analysis revealed that TRIM47 exerts an inhibitory effect on p53 and an facilitatory effect on NF-κB, thereby promoting tumor proliferation and metastasis. Taken together, TRIM47 acts as a tumor oncogene in NSCLC. Our data provide insight into the possible biological mechanism of TRIM47 in the progression of NSCLC and highlight its usefulness as a potential therapeutic target.

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