Abstract
Far less has been unveiled about the functions of lncRNAs on cancers yet. Here, we reported that lncRNA FAM87A, as a ceRNA of miR-424-5p, played a vital role in glioma development. qRT-PCR result indicated that FAM87A was abnormally downregulated in glioma tissue and cells. Survival analysis suggested that the FAM87A expression was negatively correlated with the survival rate. Effects of FAM87A on human glioma cell lines were also analyzed by MTT, Edu, and transwell assays. FAM87A hastened proliferation and migration of glioma cells. MiR-424-5p, predicted target of FAM87A, was fostered in glioma, which was examined by qRT-PCR. A negative correlation was indicated between FAM87A and miR-424-5p. Results of bioinformatics, dual luciferase, and RIP assays unveiled that FAM87A and miR-424-5p act upon each other. In addition, miR-424-5p targeted 3′-UTR of PPM1H. Also, effects of miR-424-5p/FAM87A on glioma cells were identified via the cell function experiments. FAM87A suppressed PPM1H by binding to miR-424-5p competitively, thereby restraining cell proliferation, migration, and invasion. Collectively, these findings illuminated a new mechanism for glioma progression. Therefore, FAM87A may act as a feasible target for glioma treatment.
Highlights
Glioma comprises approximately 80% of primary malignant brain tumors [1]
Through the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis on FAM87A/miR-424-5p/PPM1H, we found that all 3 kinds of RNA were enriched in the phosphatidylinositol signaling pathway (Supplementary Figure 1)
In recent years, increasing evidence showed that long noncoding RNAs (lncRNAs) are involved in regulation of tumor progression [17]
Summary
Glioma comprises approximately 80% of primary malignant brain tumors [1]. In recent years, surgical resection combining temozolomide (TMZ) chemotherapy is generally used for the treatment of glioma [2]. LncRNAs are directly involved in the biological processes of tumors and modulate downstream target genes via competitively binding to miRNAs to achieve the regulation of oncogenesis. He et al [10] reported that lncRNA UCA1 modulates iASPP by competitively binding to miR-182, thereby regulating the proliferation and metastasis of gliomas. Bioinformatic tools were applied to predict potential miRNA targets which may interact with FAM87A to regulate glioma cell progression. We reported the FAM87A/miR-424-5p axis, which regulated glioma cell behaviors by targeting PPM1H. Our findings offer novel insights into functions of FAM87A and miR-424-5p in glioma metastasis
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