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10499824 
Journal Article 
Upregulation of lncRNA HAGLROS enhances the development of nasopharyngeal carcinoma via modulating miR-100/ATG14 axis-mediated PI3K/AKT/mTOR signals 
Zhang, W; Zhang, Y; Xi, S 
2019 
Artificial Cells, Nanomedicine, and Biotechnology
ISSN: 2169-1401
EISSN: 2169-141X 
47 
1 
3043-3052 
English 
31334669 
WOS:000476899000001 
has retraction 7336185 Expression of Concern:(Artificial Cells, Nanomedicine, and Biotechnology, (2019), 47, 1, (3043-3052), 10.1080/21691401.2019.1640233)
has retraction 10507790 (Retraction of Vol 47, Pg 3043, 2019)
We planned to dig the significant role of long noncoding RNA HAGLROS in nasopharyngeal carcinoma (NPC) and the latent mechanism. The levels of HAGLROS in NPC tissues and cells were determined, followed by correlation analysis of HAGLROS level and clinicopathological features of patients suffered with NPC. The impacts of HAGLROS dysregulation on NPC cell viability, apoptosis, and the expression of apoptotic proteins and autophagy-related symbols were investigated. Moreover, we explored whether HAGLROS modulated the expression of autophagy-related gene 14 (ATG14) by competitively sponging miR-100, and then regulated the briskness of PI3K/AKT/mTOR signals in NPC development. HAGLROS level in NPC tissues and cell was very high. High level of HAGLROS indicated a short overall survival in NPC patients. Depressing of HAGLROS lessened NPC cell viability, enhanced apoptosis and reduced autophagy. Besides, HAGLROS negative controlled miR-100 and consequently targeted ATG14 expression, thus modulating NPC cell viability, apoptosis, and autophagy. Besides, dysregulation of HAGLROS/miR-100/ATG14 axis was correlated to the briskness of PI3K/AKT/mTOR signals in NPC cells. Our results indicate that of the augment of HAGLROS contributes to NPC development via modulating miR-100/ATG14 axis-mediated PI3K/AKT/mTOR signals. Our study will offer a comprehensive basis for better illustrating the pathogenesis of NPC. Highlights HAGLROS expression was upregulated in NPC tissues and cells. High expression of HAGLROS indicated a short overall survival in NPC patients. Silencing of HAGLROS promoted apoptosis and inhibited autophagy of NPC cells. HAGLROS regulated ATG14 expression in NPC cells via sponging miR-100. HAGLROS/miR-100/ATG14 axis regulated NPC development via PI3K/AKT/mTOR pathway.