Research Papers:
Long noncoding RNA AB073614 promotes the malignance of glioma by activating Wnt/β-catenin signaling through downregulating SOX7
Metrics: PDF 1586 views | HTML 2513 views | ?
Abstract
Yuqian Li1,*, Gang Zhu1,*, Wen Zeng1,*, Jiancai Wang1, Zhihong Li1, Bao Wang1, Bo Tian1, Dan Lu1, Xingye Zhang1, Guodong Gao1 and Lihong Li1
1Department of Neurosurgery, Tangdu Hospital, The Fourth Military Medical University, Xi’an, Shaanxi, 710038, China
*These authors contributed equally to this work
Correspondence to:
Lihong Li, email: [email protected]
Guodong Gao, email: [email protected]
Keywords: AB073614, glioma, long noncoding RNA, SOX7, Wnt/β-catenin
Received: April 03, 2017 Accepted: June 28, 2017 Published: July 17, 2017
ABSTRACT
Long noncoding RNA (lncRNA) AB073614 has recently shown to be aberrantly increased and identified as a poor prognostic biomarker in human glioma. However, the potential mechanisms remain unknown. This study demonstrated that AB073614 expression was significantly upregulated in both glioma tissues and cell lines, and glioma patients with high AB073614 expression had lower overall survival rates. Importantly, silencing AB073614 expression remarkably inhibited U251 cell proliferation, migration, and invasion in vitro, as well as suppressed tumor formation in vivo. The level of AB073614 was found to correlate inversely with sex-determining region Y-box 7 (SOX7) expression but correlate positively with Wnt/β-catenin signaling activity. Of note, the data showed that the inhibition of SOX7 could reverse the tumor-suppressive effect of the silencing AB073614 on glioma in vitro and in vivo. Furthermore, the results indicated that AB073614 induced Wnt/β-catenin signaling activity by repressing SOX7 expression. In conclusion, the findings demonstrated that AB073614 promoted the progression of glioma by targeting SOX7 to activate the Wnt/β-catenin signaling pathway, suggesting that the inhibition of AB073614 might be a potential target for therapeutic intervention in glioma patients.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 19305