miR-1323 inhibits bladder cancer growth by targeting PMEPA1

Background Bladder cancer is one of the common malignant tumors in the urinary system, and its incidence has been increasing year by year in recent years. However, effective treatment options for advanced bladder cancer are still lacking at present. The molecular mechanisms underlying the occurrence and development of bladder cancer have not been fully elucidated. Previous studies have found that various genes are abnormally regulated in bladder cancer tumor tissues, and the abnormal expression of microRNAs also affects protein expression. Methods The analysis of the TCGA-BLCA dataset was used to identify differentially expressed genes in bladder cancer. RT-qPCR and Western blot were used to detect the expression levels of PMEPA1, miR-1323, and SMAD/p-SMAD proteins. The CCK-8 assay and wound healing assay were used to evaluate cell proliferation and migration. Flow cytometry with AnnexinⅤ-FITC/PI double labeling was used to detect apoptosis. The interaction between miR-1323 and PMEPA1 was verified by Dual Luciferase Reporter Assay. Results: The results indicate that PMEPA1 is upregulated in bladder cancer tissues and cells. High expression of PMEPA1 stimulates bladder cancer cell proliferation and migration while inhibiting apoptosis. Databases such as TargetScan_8.0 predicted and Dual Luciferase Reporter Assay and Western blot experiments verified the interaction between miR-1323 and PMEPA1. Knockdown of miR-1323 promotes bladder cancer cell proliferation and migration, inhibits apoptosis, and reduces the expression of SMAD2/SMAD3 and p-SMAD2/p-SMAD3 proteins, while simultaneous knockdown of PMEPA1 can counteract these changes induced by miR-1323 knockdown. Conclusions: In summary, miR-1323 can inhibit bladder cancer progression by targeting PMEPA1, potentially through suppression of the SMAD-dependent TGF-β signaling pathway. Both miR-1323 and PMEPA1 may serve as potential therapeutic targets for bladder cancer.