MicroRNA-1296 expression is associated with prognosis and inhibits cell proliferation and invasion by Wnt signaling in non-small cell lung cancer

MicroRNA-1296 表达与非小细胞肺癌预后相关,并通过 Wnt 信号抑制细胞增殖和侵袭

阅读:8
作者:Haiqing Deng, Changping Xie, Yi Ye, Zhenglong Du

Abstract

MicroRNAs (miRNAs) are vital regulators of non-small cell lung cancer (NSCLC) development and tumorigenesis. The aim of the present study was to explore the role of miRNA (miR)-1296 expression in NSCLC. The expression of miR-1296 was detected by reverse transcription-quantitative PCR in NSCLC tissues and matched normal tissues. The association of miR-1296 expression with clinicopathological factors of NSCLC patients was evaluated by the χ2 test. Prognostic value of miR-1296 expression levels in patients with NSCLC was assessed using the Kaplan-Meier method and a Cox proportional hazards model; Cell Counting Kit-8, Transwell migration and western blot assays were used to detect the association between miR-1296 and cell proliferation, invasion and Wnt signaling in NSCLC, respectively. The results of the present study demonstrated that miR-1296 expression was significantly downregulated in NSCLC tissues and cells compared to corresponding controls. Lower miR-1296 expression exhibited a significant association with lymph node metastasis and tumor-node-metastasis stage of patients with NSCLC. In addition, the survival analysis demonstrated that low miR-1296 expression predicted a poorer prognosis compared to high miR-1296 expression. Multivariate Cox analysis also demonstrated that reduced miR-1296 expression was an independent risk factor of NSCLC prognosis. Additionally, miR-1296 inhibited cell proliferation, invasion and Wnt signaling in NSCLC. Thus, the results of the present study indicated that miR-1296 expression may be a potential biomarker of NSCLC prognosis and potential target for NSCLC treatment.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。