Down‐regulation of the long noncoding RNA‐HOX transcript antisense intergenic RNA inhibits the occurrence and progression of glioma

• Published in: Journal of cellular biochemistry Vol. 119; no. 2; pp. 2278 - 2287
• Main Authors: Yang, Bin, Wei, Zhen‐Yu, Wang, Bang‐Qing, Yang, Hua‐Chao, Wang, Jun‐Yi, Bu, Xing‐Yao
• Format: Journal Article
• Language: English
• Published: United States 01-02-2018
• Subjects: Animals; Apoptosis; Brain Neoplasms - genetics; cell apoptosis; cell invasion; Cell Line, Tumor; cell migration; Cell Movement; cell proliferation; Disease Progression; Down-Regulation; Gene Expression Regulation, Neoplastic; Glioma - genetics; glioma cell; Humans; long non coding; Mice; Neoplasm Transplantation; RNA, Long Noncoding - genetics; RNA‐HOX transcript antisense intergenic RNA; glioma cell; cell proliferation; RNA-HOX transcript antisense intergenic RNA; long non coding; cell apoptosis; cell migration; cell invasion
• ISSN: 0730-2312; 1097-4644
• DOI: 10.1002/jcb.26390

This study aims to explore the role of long noncoding RNA (lncRNA)‐HOX transcript antisense intergenic RNA (HOTAIR) in the occurrence and progression of glioma. Fresh glioma and normal brain tissues were classified into a glioma group (n = 67) and a normal group (n = 64) respectively. U87 cells were assigned into the blank, sh‐NC, and sh‐HOTAIR groups. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was utilized to determine HOTAIR expression. Cell proliferation, cell cycle and cell apoptosis rates were detected by cell counting kit‐8 (CCK‐8) and flow cytometry (FCM). Scratch test and transwell assay were conducted for cell migration and invasion. Orthotopic glioma tumor model in nude mice was established by inoculating tumor cell suspension. Hematoxylin‐Eosin (HE) staining was used to observe the growth and invasion of orthotopic glioma tumors. The expression of HOTAIR and cell viability was found to be lowest in the sh‐HOTAIR group among the three groups. The sh‐HOTAIR group exhibited a higher apoptotic rate and lower number of cell migration compared with the blank and sh‐NC groups. Additionally, the speed of wound healing was slower, the migration distance decreased and the survival time of nude mice was extended in the sh‐HOTAIR compared to the other groups. Moreover, the sh‐HOTAIR group demonstrated reduced lesion sizes and inflammation, no convulsions or hemiplegia and lesser number of satellite metastases. Our findings support that down‐regulation of HOTAIR could inhibit cell proliferation, promote cell apoptosis as well as suppress cell invasion and migration in the progression of glioma.
Our findings support that down‐regulation of HOTAIR could inhibit cell proliferation, promote cell apoptosis as well as suppress cell invasion and migration in the progression of glioma.