Long non-coding RNA DPP10-AS1 represses the proliferation and invasiveness of glioblastoma by regulating miR-24-3p/CHD5 signaling pathway

Objective: This investigation aimed to unveil new prospective diagnosis-related biomarkers together with treatment targets against glioblastoma. Methods: The expression levels of long non-coding RNA (lncRNA) DPP10AS1 were assessed using real-time quantitative polymerase chain reaction (RT-qPCR) within both the patient tissue specimens and glioblastoma cell lines. The relationship between lncRNA DPP10-AS1 expression in glioblastoma and patient prognosis was investigated. Cell Counting Kit-8 (CCK-8), transwell, and clonogenic experiments were utilized to assess tumor cells' proliferation, invasiveness, and migratory potentials after lncRNA DPP10-AS1 expression was up or down-regulated. Using an online bioinformatics prediction tool, the intracellular localization of lncRNA DPP10-AS1 and its target miRNA were predicted, and RNA-FISH verified results. A dual-luciferase reporter experiment validated the relationship across miR-24-3p together with lncRNA DPP10-AS1. MiR-24-3p expression within glioblastoma was identified through RT-qPCR, and potential link across miR-24-3p and lncRNA DPP10-AS1 was assessed using Pearson correlation analysis. Moreover, influence from lncRNA DPP10-AS1/miR-24-3p axis upon glioblastoma cell progression was assessed in vivo via a subcutaneous xenograft tumor model. Results: The expression of lncRNA DPP10-AS1 was notably reduced in both surgical specimens of glioblastoma and the equivalent cell lines. Low level of lncRNA DPP10-AS1 in glioblastoma is following poor prognosis. The downregulation of lncRNA DPP10-AS1 in glioblastoma cells resulted in enhanced cellular proliferation, migration, and invasion capabilities, accompanied by downregulated E-cadherin and upregulated vimentin and N-cadherin. Additionally, the observed upregulation of lncRNA DPP10-AS1 demonstrated a substantial inhibitory function upon proliferation, invasion, and migratory capabilities of LN229 cells. Subcellular localization disclosed that lncRNA DPP10-AS1 had a binding site that interacted with miR-24-3p. Upregulated miR-24-3p was detected in glioblastomas, displaying an inverse correlation with lncRNA DPP10-AS1 expression. MiR-24-3p downstream target has been determined as chromodomain helicase DNA binding protein 5 (CHD5). LncRNA DPP10-AS1 affected the invasion and proliferation of glioblastoma by controlling the miR-24-3p/CHD5 axis. Conclusion: The present study demonstrated that lncRNA DPP10-AS1 can inhibit the invasive, migratory, and proliferative properties of glioblastoma by regulating the miR-243p/CHD5 signaling pathway. Consequently, lncRNA DPP10-AS1 has potential as a tumor suppressor and might be utilized for accurate diagnosis and targeted treatments of glioblastomas.