4.7 Article

LINC01393, a Novel Long Non-Coding RNA, Promotes the Cell Proliferation, Migration and Invasion through MiR-128-3p/NUSAP1 Axis in Glioblastoma

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Publisher

MDPI
DOI: 10.3390/ijms24065878

Keywords

competing endogenous RNA; glioblastoma; LINC01393; miR-128-3p; nucleolar and spindle-associated protein 1

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This study investigates the upstream regulatory lncRNAs and miRNAs of NUSAP1, a potential molecular marker and intervention target for glioblastoma. Multiple databases were used to screen for upstream lncRNAs and miRNAs of NUSAP1, and in vitro and in vivo experiments were conducted to elucidate their biological significance and regulatory mechanism. Clinical specimens confirmed the negative correlations between LINC01393 and miR-128-3p. Further experiments validated the LINC01393/miR-128-3p/NUSAP1 interactions. The study deepens understanding of GBM mechanisms and provides potential novel therapeutic targets.
Nucleolar and spindle-associated protein 1 (NUSAP1) is a potential molecular marker and intervention target for glioblastoma (GBM). In this study, we aim to investigate upstream regulatory lncRNAs and miRNAs of NUSAP1 through both experimental and bioinformatic methods. We screened upstream lncRNAs and miRNAs of NUSAP1 through multiple databases based on ceRNA theory. Then, in vitro and in vivo experiments were performed to elucidate the relevant biological significance and regulatory mechanism among them. Finally, the potential downstream mechanism was discussed. LINC01393 and miR-128-3p were screened as upstream regulatory molecules of NUSAP1 by TCGA and ENCORI databases. The negative correlations among them were confirmed in clinical specimens. Biochemical studies revealed that overexpression or knockdown of LINC01393 respectively enhanced or inhibited malignant phenotype of GBM cells. MiR-128-3p inhibitor reversed LINC01393 knockdown-mediated impacts on GBM cells. Then, dual-luciferase reporter assay and RNA immunoprecipitation assay were conducted to validate LINC01393/miR-128-3p/NUSAP1 interactions. In vivo, LINC01393-knockdown decreased tumor growth and improved mice survival, while restoration of NUSAP1 partially reversed these effects. Additionally, enrichment analysis and western blot revealed that the roles of LINC01393 and NUSAP1 in GBM progression were associated with NF-kappa B activation. Our findings showed that LINC01393 sponged miR-128-3p to upregulate NUSAP1, thereby promoting GBM development and progression via activating NF-kappa B pathway. This work deepens understanding of GBM mechanisms and provides potential novel therapeutic targets for GBM.

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