Abstract
BackgroundPrevious 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).MethodsThe 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.ResultsHLA-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.ConclusionHLA-F-AS1 may sponge MEG3 in GBM cells to promote cell invasion and migration, and to suppress cell apoptosis.
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