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


1 Department of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China
2 Department of Neurosurgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu, 233000, China

* Corresponding Author: JUN DONG. Email: email

BIOCELL 2023, 47(12), 2721-2733.


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) DPP10-AS1 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 up-regulation 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-24-3p/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.


Cite This Article

SUN, J., XU, L., ZHANG, Y., LI, H., FENG, J. et al. (2023). Long non-coding RNA DPP10-AS1 represses the proliferation and invasiveness of glioblastoma by regulating miR-24-3p/CHD5 signaling pathway. BIOCELL, 47(12), 2721–2733.

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