Dataset Information

Long non-coding RNA PSMA3-AS1 enhances cell proliferation, migration and invasion by regulating miR-302a-3p/RAB22A in glioma.

ABSTRACT: Glioma is the most prevalent solid tumor in the central nervous system (CNS). Recently, it has been indicated that long non-coding RNAs (lncRNAs) substantially adjust the development of a variety of human cancers. In the present study, it was found and verified via microarray analysis that lncRNA PSMA3-AS1 exhibited a high expression in glioma tissues and cell lines. Then CCK-8, 5-Ethynyl-2'-deoxyuridine (EdU) staining, plate clone assay, Transwell assay, Western blotting and nude mouse model were adopted to verify PSMA3-AS1's effects on glioma. Knockdown of PSMA3-AS1 inhibited the migration, proliferation and invasion of glioma cells in vivo and in vitro. Besides, PSMA3-AS1 bound to miR-302a-3p directly reduced the expression of miR-302a-3p, thus functioning as an endogenous sponge confirmed by luciferase reporter assay and bioinformatics analysis. PSMA3-AS1 knockdown remarkably enhanced the role of miR-302a-3p overexpression in cell behaviors in glioma. Moreover, these assays also confirmed that RAB22A was a target of miR-302a-3p. In this research, therefore, the PSMA3-AS1/miR-302a-3p/RAB22A pathway regulatory axis may be revealed in the pathogenesis of glioma, and PSMA3-AS1 can be used as an underlying target for the treatment and prognosis of glioma.

SUBMITTER: Zhou LL

PROVIDER: S-EPMC7507598 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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Long non-coding RNA PSMA3-AS1 enhances cell proliferation, migration and invasion by regulating miR-302a-3p/RAB22A in glioma.

Zhou Li-Li LL Zhang Meng M Zhang Yan-Zhen YZ Sun Mei-Fen MF

Bioscience reports 20200901 9

Glioma is the most prevalent solid tumor in the central nervous system (CNS). Recently, it has been indicated that long non-coding RNAs (lncRNAs) substantially adjust the development of a variety of human cancers. In the present study, it was found and verified via microarray analysis that lncRNA PSMA3-AS1 exhibited a high expression in glioma tissues and cell lines. Then CCK-8, 5-Ethynyl-2'-deoxyuridine (EdU) staining, plate clone assay, Transwell assay, Western blotting and nude mouse model we ...[more]

PMID: 32894281

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Project description:BackgroundThe present study is aimed at exploring the specific expression of miR-193a-3p and the mechanism underlying miR-193a-3p-mediated mesenchymal transition (MT), invasion, and migration in glioma.MethodsThe gene expression profile datasets of GSE39486 and GSE25676 were downloaded from the National Center for Biotechnology (NCBI). Data regarding the expression of miR-193a-3p and survival curves were derived from Chinese Glioma Genome Atlas (CGGA). Online websites including miRWalk, DIANA, and starbase were employed to predict the target genes for miR-193a-3p. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed by the Omicsbean online software. Module analysis of the protein-protein interaction (PPI) networks was performed by the plug-in Molecular Complex Detection (MCODE), and the degrees of genes were calculated by CytoHubba plug-in of Cytoscape. Survival curves were based on the Gene Expression Profile Interaction Analysis (GEPIA). Transwell, wound healing, and Western blot experiments were performed to investigate the effects of miR-193a-3p and beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC) on the invasion, migration, and MT of glioma.ResultsmiR-193a-3p was highly expressed in glioma tissues and significantly correlated with poor survival in patients with glioma. The target genes for miR-193a-3p were involved in many cancer-related signaling pathways. The PPI showed 11 genes with both high degrees and MCODE scores in the network. Survival analysis demonstrated that the expression of BTRC was significantly correlated with the prognosis of patients with glioma. The results from the transwell, wound healing, and Western blot analyses suggested that miR-193a-3p promoted the invasion, migration, and MT of glioma cells, which could be reversed by BTRC.ConclusionsmiR-193a-3p was upregulated in patients with glioma and could affect the invasion, migration, and MT of glioma by regulating BTRC.

Project description:Rationale: Glioma is the most common primary malignant tumor of human central nervous system, and its rich vascular characteristics make anti-angiogenic therapy become a therapeutic hotspot. However, the existence of glioma VM makes the anti-angiogenic therapy ineffective. SUMOylation is a post-translational modification that affects cell tumorigenicity by regulating the expression and activity of substrate proteins. Methods: The binding and modification of IGF2BP2 and SUMO1 were identified using Ni2+-NTA agarose bead pull-down assays, CO-IP and western blot; and in vitro SUMOylation assays combined with immunoprecipitation and immunofluorescence staining were performed to explore the detail affects and regulations of the SUMOylation on IGF2BP2. RT-PCR and western blot were used to detect the expression levels of IGF2BP2, OIP5-AS1, and miR-495-3p in glioma tissues and cell lines. CCK-8 assays, cell transwell assays, and three-dimensional cell culture methods were used for evaluating the function of IGF2BP2, OIP5-AS1, miR-495-3p, HIF1A and MMP14 in biological behaviors of glioma cells. Meantime, RIP and luciferase reporter assays were used for inquiring into the interactions among IGF2BP2, OIP5-AS1, miR-495-3p, HIF1A and MMP14. Eventually, the tumor xenografts in nude mice further as certained the effects of IGF2BP2 SUMOylation on glioma cells. Results: This study proved that IGF2BP2 mainly binds to SUMO1 and was SUMOylated at the lysine residues K497, K505 and K509 sites, which can be reduced by SENP1. SUMOylation increased IGF2BP2 protein expression and blocked its degradation through ubiquitin-proteasome pathway, thereby increasing its stability. The expressions of IGF2BP2 and OIP5-AS1 were up-regulated and the expression of miR-495-3p was down-regulated in both glioma tissues and cells. IGF2BP2 enhances the stability of OIP5-AS1, thereby increasing the binding of OIP5-AS1 to miR-495-3p, weakening the binding of miR-495-3p to the 3'UTR of HIF1A and MMP14 mRNA, and ultimately promoting the formation of VM in glioma. Conclusions: This study first revealed that SUMOylation of IGF2BP2 regulated OIP5-AS1/miR-495-3p axis to promote VM formation in glioma cells and xenografts growth in nude mice, providing a new idea for molecular targeted therapy of glioma.

Dataset Information

Long non-coding RNA PSMA3-AS1 enhances cell proliferation, migration and invasion by regulating miR-302a-3p/RAB22A in glioma.

Publications

Long non-coding RNA PSMA3-AS1 enhances cell proliferation, migration and invasion by regulating miR-302a-3p/RAB22A in glioma.

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