Urinary exosomal lnc-TAF12–2:1 promotes bladder cancer progression through the miR-7847–3p/ASB12 regulatory axis

Exosomes encompass a great deal of valuable biological information and play a critical role in tumor development. However, the mechanism of exosomal lncRNAs remains poorly elucidated in bladder cancer (BCa). In this study, we identified exosomal lnc-TAF12–2:1 as a novel biomarker in BCa diagnosis and aimed to investigate the underlying biological function. Dual luciferase reporter assay, RNA immunoprecipitation (RIP), RNA pulldown assays, and xenograft mouse model were used to verify the competitive endogenous RNA mechanism of lnc-TAF12–2:1. We found exosomal lnc-TAF12–2:1 up-regulated in urinary exosomes, tumor tissues of patients, and BCa cells. Down-regulation of lnc-TAF12–2:1 impaired BCa cell proliferation and migration, and promoted cell cycle arrest at the G0/G1 phase and cell apoptosis. The opposite effects were also observed when lnc-TAF12–2:1 was overexpressed. lnc-TAF12–2:1 was transferred by intercellular exosomes to modulate malignant biological behavior. Mechanistically, lnc-TAF12–2:1 packaged in the exosomes relieved the miRNA-mediated silence effect on ASB12 via serving as a sponger of miR-7847–3p to accelerate progression in BCa. ASB12 was also first proved as an oncogene to promote cell proliferation and migration and depress cell cycle arrest and cell apoptosis in our data. In conclusion, exosomal lnc-TAF12–2:1, located in the cytoplasm of BCa, might act as a competitive endogenous RNA to competitively bind to miR-7847–3p, and then be involved in miR-7847–3p/ASB12 regulatory axis to promote tumorigenesis, which provided a deeper insight into the molecular mechanism of BCa.