Expression of lncRNA FAM95B1 in glioma and the possible mechanism of its effect on the proliferation and migration of LN382 cells
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Abstract:
Objective: To explore the effects of long-chain non-coding RNA (lncRNA) FAM95B1 on the proliferation and migration of glioma cells and explore its related mechanisms. Methods: The glioma tissues and corresponding para-cancerous tissues of 38 glioma patients who underwent surgical treatment in The Third People's Hospital of Hefei from January 2018 to August 2020 were selected for this study. qPCR was used to detect the expression level of FAM95B1 in glioma tissues and cell lines. LN382 cells with the lowest FAM95B1 expression were used as the research object and transfected with empty plasmid (control group) or pcDNA3.1-FAM95B1 plasmid (experimental group). MTT assay and Scratch test were used to detect the effect of FAM95B1 on the proliferation and migration of LN382 cells. Bioinformatics tools were used to predict the relationship among FAM95B1, miR-26a-5p, and the phosphatase and tensin homology deleted on chromosome ten (PTEN), which was further verified by Dual-luciferase reporter gene assay. qPCR and Western blotting were used to detect the effect of FAM95B1 on the expression of miR-26a-5p and PTEN. Results:The expression of FAM95B1 in glioma tissues was significantly lower than that in para-cancerous tissues (P<0.01). The expression of FAM95B1 in various glioma cell lines was significantly lower than that in normal brain glial cells (all P<0.01). Overexpression of FAM95B1 could inhibit the proliferation (P<0.05) and migration ability (P<0.01) of LN382 cells. FAM95B1 could complementarily bind with miR-26a-5p (P<0.01), and miR-26a-5p could complementarily bind with PTEN mRNA (P<0.01). Overexpression of FAM95B1 could down-regulate the expression of miR-26a-5p (P<0.01),and promote the mRNA and protein expression of PTEN (P<0.01) in LN382 cells. Conclusion: The abnormally low expression of FAM95B1 in glioma tissues and cell lines inhibits the expression of miR-26a-5p by exerting the function of competitive endogenous RNA to enhance PTEN gene expression, and inhibits the proliferation and migration of glioma cell line LN382.
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Project supported by the National Natural Science Foundation of China (No.81672477)