J Cancer 2020; 11(19):5700-5712. doi:10.7150/jca.46381 This issue

Research Paper

LINC00662 sponges miR-107 accelerating the invasiveness and proliferation of glioma cells

Jinsong Wu, Xiaolong Guo, Dongxiao Xu, Hongri Zhang

Department of Neurosurgery, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang 471003 Henan China.

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Wu J, Guo X, Xu D, Zhang H. LINC00662 sponges miR-107 accelerating the invasiveness and proliferation of glioma cells. J Cancer 2020; 11(19):5700-5712. doi:10.7150/jca.46381. Available from https://www.jcancer.org/v11p5700.htm

File import instruction


Increasing evidence revealed that the aberrant expression of long non-coding RNAs (lncRNAs) has been implicated in tumorigenesis. However, the role and mechanisms of LINC00662 in glioma have not been elucidated. Here, we show that upregulation of LINC00662 expression in glioma is associated with advanced clinical features and poor prognosis. Our results from loss-of-function assays suggest that LINC00662 silencing suppresses the proliferative and invasive abilities of glioma cells. In vivo, glioma growth was inhibited by depletion of LINC00662 in nude mice. Mechanistically, LINC00662 directly interacts with miR-107. The High-mobility group box 1 protein (HMGB1) is a known target of miR-107. Moreover, rescue assays reveal that HMGB1 overexpression (or miR-107 inhibition) reverses the glioma growth inhibition caused by LINC00662 knockdown. In conclusion, our results indicate that LINC00662 acts as an oncogene in glioma by modulating the miR-107/HMGB1 axis, suggesting that LINC00662 could be a novel therapeutic target for glioma treatment.

Keywords: glioma, LINC00662, miR-107, HMGB1, ceRNA