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Hsa-miR-134 suppresses non-small cell lung cancer (NSCLC) development through down-regulation of CCND1

Cheng-Cao Sun _, Shu-Jun Li and De-Jia Li

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Oncotarget. 2016; 7:35960-35978. https://doi.org/10.18632/oncotarget.8482

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Abstract

Cheng-Cao Sun1, Shu-Jun Li1,2, De-Jia Li1

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

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

Correspondence to:

De-Jia Li, email: [email protected]

Keywords: hsa-miRNA-134 (miR-134), cyclin D1, non-small cell lung cancer (NSCLC), proliferation, apoptosis

Received: November 29, 2015     Accepted: April 18, 2016     Published: June 14, 2016

ABSTRACT

Hsa-miRNA-134 (miR-134) has recently been discovered to have anticancer efficacy in different organs. However, the role of miR-134 on non-small cell lung cancer (NSCLC) is still ambiguous. In this study, we investigated the role of miR-134 on the development of NSCLC. The results indicated that miR-134 was significantly down-regulated in primary tumor tissues and very low levels were found in NSCLC cell lines. Ectopic expression of miR-134 in NSCLC cell lines significantly suppressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibition of cyclin D1, cyclin D2, CDK4 and up-regulation of p57(Kip2) and p21(Waf1/Cip1). In addition, miR-134 induced apoptosis, as indicated by concomitantly with up-regulation of key apoptosis protein cleaved caspase-3, and down-regulation of anti-apoptosis protein Bcl2. Moreover, miR-134 inhibited cellular migration and invasiveness through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene CCND1 was revealed to be a putative target of miR-134, which was inversely correlated with miR-134 expression in NSCLC. Taken together, our results demonstrated that miR-134 played a pivotal role on NSCLC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic CCND1.


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