Abstract
Glioma is among the most aggressive of all human malignancies. Long non-coding RNA (lncRNA) gastric carcinoma highly expressed transcript 1 (GHET1) was considered an important oncogene in tumors. However, the role of GHET1 in glioma was rarely studied. The present work aimed to explore the effect of GHET1 on glioma cell line U251. The viability, migration and invasion of U251 cells were analyzed by Cell Counting Kit-8 (CCK-8) assay, and transwell migration/invasion assay, respectively. The relative expression of GHET1 and miR-216a were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The expression of cell cycle-related proteins, cell metastasis-associated proteins and main factors in the JAK2/STAT3 and p53/survivin pathways was analyzed by Western blot. Cell transfection assay was conducted to alter expression of GHET1 and miR-216a in U251 cells. The viability, migration and invasion of U251 cells were promoted by GHET1 overexpression. The pro-cell cycle genes including Cyclin D1, CDK4 and CDK6, and the pro-metastasis genes including MMP-9 and Vimentin were up-regulated after GHET1 was overexpressed. MiR-216a was found to be down-regulated by GHET1 overexpression, and it was involved in the effects of GHET1 on U251 cells. GHET1 might promote U251 cells by down-regulating miR-216a. Finally, we found that GHET1 overexpression activated the JAK2/STAT3 and p53/survivin signaling pathways by down-regulating miR-216a. GHET1 overexpression increased viability, migration and invasion of U251 cells by down-regulating miR-216a. Mechanically, GHET1-miR-216a axis activated the JAK2/STAT3 and p53/survivin signaling pathways.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: European review for medical and pharmacological sciences
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
