These authors contribute equally to this work.
Candidate tumour suppressor CCDC19 regulates miR-184 direct targeting of C-Myc thereby suppressing cell growth in non-small cell lung cancers
Article first published online: 26 JUN 2014
© 2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Journal of Cellular and Molecular Medicine
Volume 18, Issue 8, pages 1667–1679, August 2014
How to Cite
Liu, Z., Mai, C., Yang, H., Zhen, Y., Yu, X., Hua, S., Wu, Q., Jiang, Q., Zhang, Y., Song, X. and Fang, W. (2014), Candidate tumour suppressor CCDC19 regulates miR-184 direct targeting of C-Myc thereby suppressing cell growth in non-small cell lung cancers. Journal of Cellular and Molecular Medicine, 18: 1667–1679. doi: 10.1111/jcmm.12317
- Issue published online: 2 SEP 2014
- Article first published online: 26 JUN 2014
- Manuscript Accepted: 3 APR 2014
- Manuscript Received: 16 OCT 2013
- National Nature Science Fund of China. Grant Numbers: 81101781, 81071632
- Guangdong Province Breeding Project Plan. Grant Number: LYM11102
- tumour suppressor;
- lung cancer;
We previously reported and revised the nasopharyngeal epithelium specific protein CCDC19 and identified it as a potential tumour suppressor in nasopharyngeal carcinoma. The purpose of this study was to investigate the involvement of CCDC19 in the pathogenesis of human non-small cell lung cancers (NSCLC). Down-regulated CCDC19 expression was observed in NSCLC tissues and cells compared to normal tissues. However, reduced protein expression did not correlate with the status of NSCLC progression. Instead, we observed that patients with lower CCDC19 expression had a shorter overall survival than did patients with higher CCDC19 expression. Lentiviral-mediated CCDC19 overexpression significantly suppressed cell proliferation and cell cycle transition from G1 to S and G2 phases in NSCLC cells. Knocking down CCDC19 expression significantly restored the ability of cell growth in CCDC19 overexpressing NSCLC cells. Mechanistically CCDC19 functions as a potential tumour suppressor by stimulating miR-184 suppression of C-Myc thus blocking cell growth mediated by the PI3K/AKT/C-Jun pathway. Our studies are the first to demonstrate that reduced expression of CCDC19 is an unfavourable factor in NSCLC.