Research Paper|Volume 9, Issue 2|pp 475—486

Long intergenic non-protein coding RNA 00858 functions as a competing endogenous RNA for miR-422a to facilitate the cell growth in non-small cell lung cancer

Shao-Ping Zhu¹, Jun-Yu Wang², Xian-Guo Wang¹, Jin-Ping Zhao¹

¹Department of Cardiothoracic Surgery, ZhongNan Hospital of Wuhan University, 430071 Wuhan, P. R. China
²Department of Oncology, Hubei Provincial Hospital of Integrated Chinese and Western Medicine, 430015 Wuhan, P. R. China

* * Equal contribution

Received: November 27, 2016Accepted: January 31, 2017Published: February 6, 2017

Copyright: © 2017 Zhu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The expression of long non-coding RNAs (lncRNAs) is dysregulated in non-small cell lung cancer (NSCLC). However, the functions and contributions of lncRNAs remain largely unknown. Here, we identified a critical role of long intergenic non-protein coding RNA 00858 (LINC00858) in NSCLC. Ectopic expression of LINC00858 in NSCLC cells promoted cell proliferation and induced cell migration and invasion. Moreover, LINC00858 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-422a and thereby modulating the expression of kallikrein-related peptidase 4 (KLK4). In NSCLC patients, high expression of LINC00858 closely correlated with tumor progression. Thus, targeting the ceRNA network involving LINC00858 may be used as a treatment strategy against NSCLC.