Research Paper Volume 11, Issue 5 pp 1471—1485
LINC00702 suppresses proliferation and invasion in non-small cell lung cancer through regulating miR-510/PTEN axis
- 1 Department of Respiratory, the Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China
- 2 Department of Respiratory, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, China
- 3 Department of Pathology, the Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China
- 4 Department of Geriatrics, the Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China
Received: December 5, 2018 Accepted: February 22, 2019 Published: March 6, 2019https://doi.org/10.18632/aging.101846
How to Cite
Copyright: Yu 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.
Background: Long non-coding RNAs (lncRNAs) have been consistently reported to be involved in the progression of non-small cell lung cancer (NSCLC). In this study, we aimed to identify aberrantly expressed lncRNAs in NSCLC, in order to explore new therapeutic targets for NSCLC.
Methods: Two pairs of NSCLC and adjacent normal tissues were first analyzed by RNA sequencing. The expressions of LINC00702 in 40 pairs patient samples and in 4 NSCLC cell lines was measured by quantitative real-time PCR. Putative target miRNAs of LINC00702 were predicted by the bioinformatics tools. The effect of LINC00702 on tumor growth in vivo was evaluated.
Results: LINC00702 was significantly down-regulated in patients with NSCLC, which was correlated with tumor size and metastasis. In addition, overexpression of LINC00702 markedly suppressed proliferation and metastasis in NSCLC cells via inducing apoptosis in vitro and in vivo. Moreover, bioinformatics and luciferase reporter assays demonstrated that LINC00702 functioned as a competing endogenous RNA (ceRNA) for miR-510 in NSCLC, and upregulated its target gene PTEN.
Conclusion: Our results indicated that LINC00702 modulated the expression of PTEN gene by acting as a ceRNA for miR-510 in NSCLC. Therefore, LINC00702 may serve as a potential target for the diagnosis and treatment of patients with NSCLC.