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Upregulation of lncRNA HAGLROS enhances the development of nasopharyngeal carcinoma via modulating miR-100/ATG14 axis-mediated PI3K/AKT/mTOR signals.
Artif Cells Nanomed Biotechnol 2019; 47(1):3043-3052AC

Abstract

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.

Authors+Show Affiliations

a Department of Otorhinolaryngology Head and Neck Surgery, Luoyang Central Hospital , Luoyang , China.b Department of Biochemistry and Molecular Biology, Medical School, Henan University of Science and Technology , Luoyang , China.b Department of Biochemistry and Molecular Biology, Medical School, Henan University of Science and Technology , Luoyang , China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31334669

Citation

Zhang, Wei, et al. "Upregulation of lncRNA HAGLROS Enhances the Development of Nasopharyngeal Carcinoma Via Modulating miR-100/ATG14 Axis-mediated PI3K/AKT/mTOR Signals." Artificial Cells, Nanomedicine, and Biotechnology, vol. 47, no. 1, 2019, pp. 3043-3052.
Zhang W, Zhang Y, Xi S. Upregulation of lncRNA HAGLROS enhances the development of nasopharyngeal carcinoma via modulating miR-100/ATG14 axis-mediated PI3K/AKT/mTOR signals. Artif Cells Nanomed Biotechnol. 2019;47(1):3043-3052.
Zhang, W., Zhang, Y., & Xi, S. (2019). Upregulation of lncRNA HAGLROS enhances the development of nasopharyngeal carcinoma via modulating miR-100/ATG14 axis-mediated PI3K/AKT/mTOR signals. Artificial Cells, Nanomedicine, and Biotechnology, 47(1), pp. 3043-3052. doi:10.1080/21691401.2019.1640233.
Zhang W, Zhang Y, Xi S. Upregulation of lncRNA HAGLROS Enhances the Development of Nasopharyngeal Carcinoma Via Modulating miR-100/ATG14 Axis-mediated PI3K/AKT/mTOR Signals. Artif Cells Nanomed Biotechnol. 2019;47(1):3043-3052. PubMed PMID: 31334669.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Upregulation of lncRNA HAGLROS enhances the development of nasopharyngeal carcinoma via modulating miR-100/ATG14 axis-mediated PI3K/AKT/mTOR signals. AU - Zhang,Wei, AU - Zhang,Yanle, AU - Xi,Shoumin, PY - 2019/7/24/entrez PY - 2019/7/25/pubmed PY - 2019/7/25/medline KW - ATG14 KW - HAGLROS KW - Nasopharyngeal carcinoma KW - PI3K/AKT/mTOR pathway KW - miR-100 SP - 3043 EP - 3052 JF - Artificial cells, nanomedicine, and biotechnology JO - Artif Cells Nanomed Biotechnol VL - 47 IS - 1 N2 - 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. SN - 2169-141X UR - https://www.unboundmedicine.com/medline/citation/31334669/Upregulation_of_lncRNA_HAGLROS_enhances_the_development_of_nasopharyngeal_carcinoma_via_modulating_miR_100/ATG14_axis_mediated_PI3K/AKT/mTOR_signals_ L2 - http://www.tandfonline.com/doi/full/10.1080/21691401.2019.1640233 DB - PRIME DP - Unbound Medicine ER -