Oncotarget

Research Papers:

This article is currently under investigation. We strongly recommend that this article is not cited until the investigation is completed.

Hsa-miR-329 exerts tumor suppressor function through down-regulation of MET in non-small cell lung cancer

Cheng-Cao Sun, Shu-Jun Li, Feng Zhang, Jing-Yu Pan, Liang Wang, Cui-Li Yang, Yong-Yong Xi and De-Jia Li _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2016; 7:21510-21526. https://doi.org/10.18632/oncotarget.7517

Metrics: PDF 1866 views  |   HTML 2724 views  |   ?  


Abstract

Cheng-Cao Sun1, Shu-Jun Li1,2, Feng Zhang1, Jing-Yu Pan1, Liang Wang1, Cui-Li Yang1, Yong-Yong Xi1 and De-Jia Li1

1 Department of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, P. R. China

2 Wuhan Hospital for the Prevention and Treatment of Occupational Diseases, Wuhan, P. R. China

Correspondence to:

De-Jia Li, email:

Keywords: hsa-miRNA-329(miR-329); MET; non-small cell lung cancer (NSCLC); proliferation; apoptosis

Received: August 18, 2015 Accepted: February 05, 2016 Published: February 19, 2016

Abstract

MicroRNAs (miRNAs) act as key regulators of multiple cancers. Hsa-miR-329 (miR-329) functions as a tumor suppressor in some malignancies. However, its role on lung cancer remains poorly understood. In this study, we investigated the role of miR-329 on the development of lung cancer. The results indicated that miR-329 was decreased in primary lung cancer tissues compared with matched adjacent normal lung tissues and very low levels were found in a non-small cell lung cancer (NSCLC) cell lines. Ectopic expression of miR-329 in lung cancer cell lines substantially repressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibiting cyclin D1, cyclin D2 and up-regulatiing p57(Kip2) and p21(WAF1/CIP1). In addition, miR-329 promoted NSCLC cell apoptosis, as indicated by up-regulation of key apoptosis gene cleaved caspase-3, and down-regulation of anti-apoptosis gene Bcl2. Moreover, miR-329 inhibited cellular migration and invasiveness through inhibiting matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene MET was revealed to be a putative target of miR-329, which was inversely correlated with miR-329 expression. Furthermore, down-regulation of MET by siRNA performed similar effects to over-expression of miR-329. Collectively, our results demonstrated that miR-329 played a pivotal role in lung cancer through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic MET.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 7517