Abstract
Long non-coding RNA forkhead box D2 adjacent opposite strand RNA 1 (FOXD2-AS1) has emerged as a potential oncogene in several tumors. However, its biological function and potential regulatory mechanism in glioma have not been fully investigated to date. In the present study, RT-qPCR was conducted to detect the levels of FOXD2-AS1 and microRNA (miR)-506-5p, and western blot assays were performed to measure the expression of CDK2, cyclinE1, P21, matrix metalloproteinase (MMP)7, MMP9, N-cadherin, E-cadherin and vimentin in glioma cells. A luciferase reporter assay was performed to verify the direct targeting of miR-506-5p by FOXD2-AS1. Subsequently, cell viability was analyzed using the CCK-8 assay. Cell migration and invasion were analyzed using Transwell and wound healing assays, respectively. The results demonstrated that FOXD2-AS1 was significantly overexpressed in glioma cells, particularly in U251 cells. Knockdown of FOXD2-AS1 in glioma cells significantly inhibited cell proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) and regulated the expression of CDK2, cyclinE1, P21, MMP7 and MMP9. Next, a possible mechanism for these results was explored, and it was observed that FOXD2-AS1 binds to and negatively regulates miR-506-5p, which is known to be a tumor-suppressor gene in certain human cancer types. Furthermore, overexpression of miR-506-5p significantly inhibited cell proliferation, migration, invasion and EMT, and these effects could be reversed by transfecting FOXD2-AS1 into the cells. In conclusion, our data suggested that FOXD2-AS1 contributed to glioma proliferation, metastasis and EMT via competitively binding to miR-506-5p. FOXD2-AS1 may be a promising target for therapy in patients with glioma.
Highlights
Glioma is one of the most common and fatal brain tumors in adults and can be classified as grade I–IV based on the pathological characteristics of malignant tumors according to the World Health Organization classification criterion [1,2]
FOXD2-AS1 expression in SHG44, LN229 and T98G cells was slightly higher than that in human astrocyte (HA) cells (P < 0.05 in SHG44 cells, P < 0.01 in LN229 cells and P < 0.01 in T98G cells). These results indicated that FOXD2-AS1 was significantly up-regulated in glioma cells, in U251 cells
In order to determine the effects of FOXD2-AS1 on the viability of glioma cells, U251 cells were transfected with small hairpin RNA (shRNA)-FOXD2-AS1 and shRNA-negative control (NC) for 24, 48 and 72 h
Summary
Glioma is one of the most common and fatal brain tumors in adults and can be classified as grade I–IV based on the pathological characteristics of malignant tumors according to the World Health Organization classification criterion [1,2]. The molecular mechanisms that mediate the development and progression of glioma should be explored, which would be beneficial for the identification of novel and effective interventions. It is well known that the majority of transcripts in the human genome are non-protein coding [6]. Long non-coding RNAs (lncRNAs) are >200 nucleotides long and do not code for proteins [7]. LncRNAs have been reported to play crucial roles in a wide range of biological processes, including proliferation, differentiation, cell-cycle regulation, genomic expression and cell death, in different tissues and cells [8]. Numerous studies have shown that lncRNAs are aberrantly expressed in various cancer types, where they serve as oncogenes or tumor suppressors [9]
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