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Upregulation of far upstream element-binding protein 1 (FUBP1) promotes tumor proliferation and unfavorable prognosis in tongue squamous cell carcinoma.
The International Journal of Biological Markers ( IF 2 ) Pub Date : 2020-04-27 , DOI: 10.1177/1724600820912252
Yang Chen 1 , Jiameng Liu 2 , Ningbo Geng 1 , Chongjin Feng 1
Affiliation  

BACKGROUND A well-known transcriptional regulator of the proto-oncogene c-Myc, far-upstream element (FUSE) binding protein 1 (FUBP1) has been demonstrated by previous work to be aberrantly expressed in lots of cancers and plays a critical role in tumor progression; however, its expression and function in tongue squamous cell carcinoma (TSCC) remains unclear. METHODS Evaluations with immunohistochemistry, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were performed to assess FUBP1 expression. The correlations of FUBP1 expression levels with various clinicopathological factors were evaluated with univariate and multivariate analyses. In addition, the role of FUBP1 in TSCC proliferation was studied in TSCC cells by silencing FUBP1. The role of FUBP1 on proliferation and apoptosis was confirmed by cell counting Kit-8, colony formation, cell cycle, and cell apoptosis assays. RESULTS Immunohistochemistry, qRT-PCR and Western blot results showed FUBP1 expression was higher in TSCC tissues in comparison with adjacent non-cancerous tissues (P <0.05), as well as in patients with advanced-stage disease or cervical lymph node metastasis (P<0.001). The 5-year survival rate was significantly lower in the group with high FUBP1 expression than in that with low FUBP1 expression (P=0.035). FUBP1 expression was also an independent predictor for overall survival in TSCC patients, and was closely related to poor prognosis. FUBP1 knockdown inhibited cancer cell proliferation, and induced cell cycle arrest and apoptosis. CONCLUSION FUBP1 was overexpressed in TSCC, and correlated with TSCC cell proliferation and poor prognosis. FUBP1 appears to act as a potential oncogene in TSCC, and may be considered a novel biomarker for TSCC.

中文翻译:

远上游元件结合蛋白 1 (FUBP1) 的上调促进舌鳞状细胞癌的肿瘤增殖和不良预后。

背景 先前的工作已经证明原癌基因 c-Myc 远上游元件 (FUSE) 结合蛋白 1 (FUBP1) 的一种众所周知的转录调节因子在许多癌症中异常表达并在肿瘤中起关键作用进展; 然而,其在舌鳞状细胞癌(TSCC)中的表达和功能仍不清楚。方法 使用免疫组织化学、定量实时聚合酶链反应 (qRT-PCR) 和蛋白质印迹进行评估以评估 FUBP1 的表达。FUBP1 表达水平与各种临床病理因素的相关性通过单变量和多变量分析进行评估。此外,通过沉默 FUBP1 在 TSCC 细胞中研究了 FUBP1 在 TSCC 增殖中的作用。通过细胞计数 Kit-8 证实了 FUBP1 对增殖和凋亡的作用,集落形成、细胞周期和细胞凋亡测定。结果免疫组化、qRT-PCR和Western blot结果显示,与癌旁非癌组织相比,TSCC组织中FUBP1的表达较高(P<0.05),晚期疾病或颈部淋巴结转移患者(P< 0.001)。FUBP1高表达组的5年生存率明显低于FUBP1低表达组(P=0.035)。FUBP1表达也是TSCC患者总生存期的独立预测因子,与预后不良密切相关。FUBP1 敲低抑制癌细胞增殖,并诱导细胞周期停滞和细胞凋亡。结论 FUBP1在TSCC中过表达,与TSCC细胞增殖和预后不良相关。
更新日期:2020-04-27
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