Research Paper Volume 12, Issue 12 pp 11568—11578
Integrative analysis of miRNAs-mRNAs reveals that miR-182 up-regulation contributes to proliferation and invasion of nasopharyngeal carcinoma by targeting PTEN
- 1 Department of Otorhinolaryngology Head and Neck Surgery, Air Force Medical University, XiJing Hospital, Xian, Shanxi, China
- 2 Department of Otolaryngology Head and Neck Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China
- 3 Department of Otorhinolaryngology Head and Neck Surgery, The 908th Hospital of Chinese People’s Liberation Army Joint Logistic Support Force, Nanchang, Jiangxi, China
Received: February 8, 2020 Accepted: April 28, 2020 Published: June 15, 2020https://doi.org/10.18632/aging.103316
How to Cite
Copyright © 2020 Shi 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.
Objective: Several miRNAs have been found to be abnormally expressed during nasopharyngeal carcinoma development. Nevertheless, the interaction between miRNAs and downstream genes remains unexploited. In this study, we aim to investigate miRNAs-mRNAs interaction and the mechanism of miR-182 in NPC.
Results: Integrative analysis identified several hub-miRNAs that drive NPC pathogenesis. The expression of miR-182 was notably increased in 32 NPC tissues and cell lines (CNE1 and 5-8F). Up-regulation of miR-182 was strongly correlated with poor prognosis of NPC patients. Moreover, the proliferation and invasion of NPC cells were notably increased in miR-182 mimics condition and decreased in miR-182 inhibitor condition. Furthermore, PTEN was verified to be a target of miR-182 and overexpression of PTEN could abrogate the promotion effect of miR-182 mimics on NPC invasion.
Conclusions: We identified several hub-miRNAs that may drive NPC pathogenesis. MiR-182 could promote proliferation and invasion of NPC cells via targeting PTEN, which provides a new insight into the clinical therapy of NPC.
Materials and Methods: Genome-wide miRNAs of NPC tissues was analyzed using high-throughput sequencing and bioinformatics tools. QRT-PCR experiment was conducted to measure relative expression level. Dual-luciferase reporter assay was used to verify target relationship. The proliferation and invasion of transfected cells were measured by CCK-8 and transwell assay.