LncRNA TRHDE-AS1 functions as a tumor suppressor via the miR-22-5p/DLG3 axis to regulate malignant phenotypes and predict prognosis in glioma

Long noncoding RNAs (lncRNAs) represent a significant avenue for investigating tumor molecular mechanisms and identifying potential therapeutic targets. It was aimed to explore the expression and prognostic significance of lncRNA TRHDE-AS1 in glioma, and clarify its ceRNA-mediated regulation of miR-22-5p/DLG3 axis in promoting glioma progression in vitro . Using the TCGA database and clinical glioma tissue samples ( n = 150), qRT-PCR was employed to detect the expression of TRHDE-AS1. Its prognostic value was assessed through Kaplan–Meier analysis and Cox regression analysis. The targeting interaction between TRHDE-AS1, miR-22-5p and DLG3 was confirmed by luciferase reporter assay and RNA Immunoprecipitation (RIP) experiments. Using CCK-8 and Transwell assays, the impact of TRHDE-AS1 on glioma cells’ malignant phenotypes was evaluated. To assess the influence on epithelial-mesenchymal transition (EMT), the protein levels of N-cadherin, Snail, and MMP-2 were measured via Western blot. Low expression of TRHDE-AS1 in glioma tissues correlated with patients’ malignant features, consistent with findings from the TCGA database. It was independently related to reduced overall survival. Upon TRHDE-AS1 upregulation, miR-22-5p levels significantly decreased while downstream target DLG3 expression increased in both U251 and LN229 cells. The proliferation, invasive metastatic ability and EMT of both cells were significantly reduced, which was offset by miR-22-5p overexpression. TRHDE-AS1/miR-22-5p mediated cellular phenotype alterations were restored by DLG3 again in both U251 and LN229 cells. Downregulation of TRHDE-AS1 was closely related to glioma patients’ poor prognosis. It may regulate miR-22-5p/DLG3 axis through the ceRNA mechanism to promote the malignant activity of glioma cells.