Hsa-miR-326 targets CCND1 and inhibits non-small cell lung cancer development

Chengcao Sun; Chuanfeng Huang; Shujun Li; Cuili Yang; Yongyong Xi; Liang Wang; Feng Zhang; Yunfeng Fu; Dejia Li

doi:10.18632/oncotarget.7071

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

Research Papers:

Expression of Concern

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

Hsa-miR-326 targets CCND1 and inhibits non-small cell lung cancer development

Chengcao Sun, Chuanfeng Huang, Shujun Li, Cuili Yang, Yongyong Xi, Liang Wang, Feng Zhang, Yunfeng Fu and Dejia Li _

PDF | HTML | Supplementary Files | How to cite

Oncotarget. 2016; 7:8341-8359. https://doi.org/10.18632/oncotarget.7071

Metrics: PDF 2165 views | HTML 3077 views | ?

Abstract

Chengcao Sun1,*, Chuanfeng Huang1,2,*, Shujun Li1,3, Cuili Yang1, Yongyong Xi1, Liang Wang1, Feng Zhang1, Yunfeng Fu4, Dejia Li1

1Department of Occupational and Environmental Health, School of Public Health, Wuhan University, 430071 Wuhan, P.R.China

2Department of Pharmacology, Basic Medical School, Nanyang Medical College, 473003 Nanyang, P.R.China

3Wuhan Hospital for the Prevention and Treatment of Occupational Diseases, 430071 Wuhan, P.R.China

4The Third Xiang-Ya Hospital, Central South University, 410013 Changsha, P.R.China

*These authors contributed equally to this work

Correspondence to:

Dejia Li, e-mail: [email protected]

Yunfeng Fu, e-mail: [email protected]

Keywords: Hsa-miRNA-326 (miR-326), cyclin D1, non-small cell lung cancer (NSCLC), proliferation, apoptosis

Received: August 18, 2015 Accepted: January 13, 2016 Published: January 29, 2016

ABSTRACT

Hsa-miRNA-326 (miR-326) has recently been discovered having anticancer efficacy in different organs. However, the role of miR-326 on non-small cell lung cancer (NSCLC) is still ambiguous. In this study, we investigated the role of miR-326 on the development of NSCLC. The results indicated that miR-326 was significantly down-regulated in primary tumor tissues and very low levels were found in NSCLC cell lines. Ectopic expression of miR-326 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-326 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-326 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-326, which was inversely correlated with miR-326 expression in NSCLC. Taken together, our results demonstrated that miR-326 played a pivotal role on NSCLC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic CCND1.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 7071

Publication Alerts

Research Papers:

Hsa-miR-326 targets CCND1 and inhibits non-small cell lung cancer development

Abstract