Research Papers:
Upregulation of long noncoding RNA HOXA-AS3 promotes tumor progression and predicts poor prognosis in glioma
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Abstract
Fan Wu1,2,8, Chuanbao Zhang1,2,8, Jinquan Cai3, Fan Yang1,2,8, Tingyu Liang1,2,8, Xiaoyan Yan1,2,8, Haoyuan Wang4, Wen Wang5, Jing Chen2,8 and Tao Jiang1,2,6,7,8
1Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beiijing, China
2Department of Molecular Neuropathology, Beijing Neurosurgical Institute, Capital Medical University, Beiijing, China
3Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China
4Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China
5Department of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, China
6Center of Brain Tumor, Beijing Institute for Brain Disorders, Beiijing, China
7China National Clinical Research Center for Neurological Diseases, Beiijing, China
8Chinese Glioma Genome Atlas Network (CGGA), Beiijing, China
Correspondence to:
Tao Jiang, email: [email protected]
Jing Chen, email: [email protected]
Keywords: glioma, LncRNA, HOXA-AS3, proliferation, tumorigenesis
Received: March 31, 2017 Accepted: May 11, 2017 Published: May 24, 2017
ABSTRACT
Long noncoding RNAs (lncRNAs) have recently emerged as new potentially promising therapeutic targets in many cancers. However, their prognostic value and biological functions associated with glioma remain to be elucidated. Here, High-throughput RNAseq was performed to detect the expression profiles of lncRNAs in 325 human glioma tissues. It was shown that a novel lncRNA HOXA-AS3 was one of the most significantly upregulated lncRNAs in glioma tissues. Quantitative PCR further verified the increased expression of HOXA-AS3 in patient samples and glioma cell lines. Uni and Multivariate Cox regression analysis revealed that HOXA-AS3 was an independent prognostic factor in glioma patients. Gene set enrichment analysis indicated that the gene sets correlated with HOXA-AS3 expression were involved in cell cycle progression and E2F targets. Functionally, HOXA-AS3 silencing resulted in proliferation arrest by altering cell cycle progression and promoting cell apoptosis, and impaired cell migration in glioma cells. Furthermore, the growth-inhibiting effect of HOXA-AS3 knockdown was also demonstrated in Xenograft mouse model. Our results highlight the important role of HOXA-AS3 in glioma progression, and indicate that HOXA-AS3 may be served as a valuable prognostic biomarker for glioma.
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