Dataset Information

LINC01094 Down-Regulates miR-330-3p and Enhances the Expression of MSI1 to Promote the Progression of Glioma.

ABSTRACT: Background:This study aims at probing into the expression, function, and mechanism of LINC01094 and miR-330-3p in glioma. Materials and Methods:qRT-PCR was employed to examine LINC01094 and miR-330-3p expressions in gliomas. After gain-of-function and loss-of-function models were constructed, CCK-8 and Transwell assays were used to detect the proliferation, migration and invasion of LN229 and U251 cells, respectively. Additionally, dual luciferase reporter gene assay was utilized to verify the binding site between m4iR-330-3p and LINC01094, miR-330-3p, and the 3'UTR of musashi RNA binding protein 1 (MSI1). Then, RNA pull-down, RIP, qRT-PCR and Western blot were employed to detect the regulatory relationships among LINC01094, miR-330-3p, and MSI1. Results:The expression of LINC01094 was elevated in glioma tissues and cell lines, and the high expression of LINC01094 was associated with high grade of glioma. In contrast, miR-330-3p was lowly expressed in glioma tissue. Overexpression of LINC01094 or down-regulation of miR-330-3p promoted the proliferation, migration, and invasion of glioma cells, while LINC01094 knockdown or miR-330-3p up-regulation impeded these processes. miR-330-3p was identified as a target miRNA of LINC01094, and it could be negatively regulated by LINC01094. In addition, miR-330-3p antagonized the function of LINC01094 by negatively regulating MSI1. Conclusion:LINC01094 promotes the proliferation, migration, and invasion of glioma cells by adsorbing miR-330-3p and up-regulating the expression of MSI1.

SUBMITTER: Zhu B

PROVIDER: S-EPMC7395698 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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LINC01094 Down-Regulates miR-330-3p and Enhances the Expression of MSI1 to Promote the Progression of Glioma.

Zhu Bin B Liu Wei W Liu Hongliang H Xu Qiang Q Xu Wei W

Cancer management and research 20200728

<h4>Background</h4>This study aims at probing into the expression, function, and mechanism of LINC01094 and miR-330-3p in glioma.<h4>Materials and methods</h4>qRT-PCR was employed to examine LINC01094 and miR-330-3p expressions in gliomas. After gain-of-function and loss-of-function models were constructed, CCK-8 and Transwell assays were used to detect the proliferation, migration and invasion of LN229 and U251 cells, respectively. Additionally, dual luciferase reporter gene assay was utilized ...[more]

PMID: 32801889

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Project description:BackgroundThough circular RNAs (circRNAs) are the key regulators in tumor carcinogenesis, they remain largely unexplored in hepatocellular carcinoma (HCC).MethodsThe expression of RanGAP1-derived circRNAs (circ_0063531, circ_0063534, circ_0063513, circ_0063518, circ_0063507, circ_0063723) were evaluated in eight paired HCC and normal tissues, and the correlation between circRanGAP1 (circ_0063531) expression and clinicopathological characteristics in 40 HCC patients was determined. The association between miR-27b-3p and circRanGAP1 or NRAS was predicted using bioinformatics analysis. The expression of circRanGAP1, miR-27b-3p, and NRAS were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The potential oncogenic role of circ-RanGAP1 was assessed using CCK-8, colony formation, transwell assays in vitro, subcutaneous tumor mouse model, vein tail metastatic model, and orthotopically implanted intrahepatic HCC model in vivo. Luciferase reporter and RNA immunoprecipitation (RIP) assays were used to explore the binding site between miR-27b-3p and circ-RanGAP1 or NRAS. Protein expression was detected using western blotting. The localization of miR-27b-3p and circ-RanGAP1 was investigated using fluorescence in situ hybridization (FISH). The level of immune infiltration was assessed by bioinformatics analysis, flow cytometry, and orthotopically implanted intrahepatic HCC models.ResultsHere, we found elevated circRanGAP1 in the cells and clinical tissues of patients with HCC. Increased circRanGAP1 levels are associated with enlarged tumors and the advanced stage of TNM. CircRanGAP1 promotes the growth, migration, and HCC cell invasion, concurrently with the growth and metastasis of tumors in-vivo. Moreover, circRanGAP1 is mainly located inside the cytoplasm. Mechanistically, circRanGAP1 as an oncogene promotes HCC progression by miR-27b-3p/NRAS/ERK axis, furthermore, affects the infiltration level of tumor-associated macrophages probably by sponging miR-27b-3p. Immune infiltration analysis shows that NRAS is positively correlated with the levels of CD68+ tumor-associated macrophages in HCC samples and that NRAS and CD68 are related to the poor outcome of HCC.ConclusionThese results reveal that circRanGAP1 is a HCC oncogene that function by the miR-27b-3p/NRAS/ERK axis and regulates the infiltration levels of tumor-associated macrophages by sponging miR-27b-3p. Therefore, circRANGAP1/ NRAS axis may be an important potential treatment target against HCC.

Dataset Information

LINC01094 Down-Regulates miR-330-3p and Enhances the Expression of MSI1 to Promote the Progression of Glioma.

Publications

LINC01094 Down-Regulates miR-330-3p and Enhances the Expression of MSI1 to Promote the Progression of Glioma.

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