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AURKA表达增加促进膀胱癌细胞增殖并预示不良预后。

Increased AURKA promotes cell proliferation and predicts poor prognosis in bladder cancer.

作者信息

Guo Mengjie, Lu Sicheng, Huang Hongming, Wang Yaohui, Yang Mary Q, Yang Ye, Fan Zhimin, Jiang Bin, Deng Youping

机构信息

School of Medicine and Life Sciences, Nanjing University of Chinese Medicine, Nanjing, 210023, China.

Department of Hematology, Affiliated Hospital of Nantong University, Nantong, 226001, China.

出版信息

BMC Syst Biol. 2018 Dec 14;12(Suppl 7):118. doi: 10.1186/s12918-018-0634-2.

Abstract

BACKGROUND

Bladder cancer (BC) is the most common cancer of the urinary bladder and upper tract, in which the clinical management is limited. AURKA (aurora kinase A) has been identified as an oncogene in cancer development; however, its potential role and underlying mechanisms in the progression of BC remain unknown.

RESULTS

In this study, we evaluated Aurora kinase A (AURKA) expression in patient samples by performing gene expression profiling, and found that AURKA expression levels were significantly higher in BC tissues than in normal tissues. Increased AURKA in BC was strongly associated with stage and grade. Moreover, BC patients with elevated AURKA achieved poor overall survival rates. The experiments in vitro comprehensively validated the critical role of AURKA in promoting BC cell proliferation using the methods of gene overexpression and gene silencing. Furthermore, we proved that AURKA inhibitor MLN8237 arrested BC cell growth and induced apoptosis.

CONCLUSIONS

These findings implicate AURKA acting as an effective biomarker for BC detection and prognosis, as well as therapeutic target.

摘要

背景

膀胱癌(BC)是膀胱和上尿路最常见的癌症,其临床治疗手段有限。极光激酶A(AURKA)已被确定为癌症发展过程中的一种致癌基因;然而,其在膀胱癌进展中的潜在作用和潜在机制仍不清楚。

结果

在本研究中,我们通过进行基因表达谱分析评估了患者样本中极光激酶A(AURKA)的表达,发现膀胱癌组织中AURKA的表达水平显著高于正常组织。膀胱癌中AURKA的增加与分期和分级密切相关。此外,AURKA升高的膀胱癌患者总生存率较差。体外实验通过基因过表达和基因沉默方法全面验证了AURKA在促进膀胱癌细胞增殖中的关键作用。此外,我们证明AURKA抑制剂MLN8237可阻止膀胱癌细胞生长并诱导凋亡。

结论

这些发现表明AURKA可作为膀胱癌检测、预后评估的有效生物标志物以及治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a250/6293497/401fdf32fa82/12918_2018_634_Fig1_HTML.jpg

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