Abstract
Objective: This work aims to delineate the involvement of LINC01082 in bladder cancer (BC) pathogenesis. Methods: Significant downregulation of LINC01082 in BC tissues was identified through GEO database analysis (GSE89006). Subsequent validation in GEPIA, TCGA, and clinical cohorts supported these findings. The diagnostic utility was evaluated via ROC curve analysis. Interaction between LINC01082 and miR-1269a, predicted by lncRNASNP, was confirmed by dual luciferase reporter assays. RT-qPCR measured the expression of LINC01082, miR-1269a, and EMT-related genes, while Transwell assays characterized cell migration and invasion. Results: LINC01082 was found to be significantly underexpressed in BC tissues and cell lines, with excellent diagnostic efficacy. LINC01082 can specifically bind to miR-1269a. When LINC01082 expression is silenced, BC cells exhibit increased migration and invasion capacities, accompanied by a decline in the epithelial marker E-cadherin and an upregulation of mesenchymal markers, including N-cadherin and vimentin. However, these effects can be effectively reversed by adding the miR-1269a inhibitor. Conclusion: LINC01082 can downregulate the expression of miR-1269a, thereby inhibiting the migration, invasion, and EMT of BC cells, ultimately hindering the malignant progression of tumors. This study provides new insights into its anticancer effects and molecular mechanisms. Supplementary Information: The online version contains supplementary material available at 10.1186/s12957-025-04026-3.