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LncRNA HLA-F-AS1 Enhances the Migration, Invasion and Apoptosis of Glioblastoma Cells by Targeting lncRNA MEG3

BACKGROUND: Previous studies revealed the oncogenic role of long non-coding RNA (lncRNA) HLA-F-AS1 in colon cancer and breast cancer, while its role in other cancers is unclear. We predicted the direct interaction between HLA-F-AS1 and MEG3, which is a tumor suppressor lncRNA. We then assessed the i...

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Detalles Bibliográficos
Autores principales: Wang, Yanhua, Xie, Teng, Liu, Huaming, Yu, Xiaoping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8678538/
https://www.ncbi.nlm.nih.gov/pubmed/34934358
http://dx.doi.org/10.2147/CMAR.S322351
Descripción
Sumario:BACKGROUND: Previous studies revealed the oncogenic role of long non-coding RNA (lncRNA) HLA-F-AS1 in colon cancer and breast cancer, while its role in other cancers is unclear. We predicted the direct interaction between HLA-F-AS1 and MEG3, which is a tumor suppressor lncRNA. We then assessed the interaction between HLA-F-AS1 and MEG3 in glioblastoma (GBM). METHODS: The expression levels of HLA-F-AS1 and MEG3 in GBM and paired non-tumor tissues from 60 GBM patients were analyzed by RT-qPCR. Overexpression of HLA-F-AS1 and MEG3 was achieved in GBM cells to explore the interaction between them. The direct interaction between them was confirmed by RNA pull-down assay. The roles of HLA-F-AS1 and MEG3 in cell invasion, migration and apoptosis were explored by Transwell assays and cell apoptosis assay. RESULTS: HLA-F-AS1 was highly expressed, and MEG3 was downregulated in GBM. Overexpression of HLA-F-AS1 reduced the expression levels of MEG3 while overexpression of MEG3 did not alter the expression of HLA-F-AS1. HLA-F-AS1 increased cell migration and invasion, but decreased cell apoptosis. MEG3 played opposite roles and reduced the effects of HLA-F-AS1 on cell behaviors. CONCLUSION: HLA-F-AS1 may sponge MEG3 in GBM cells to promote cell invasion and migration, and to suppress cell apoptosis.