Conclusion
AATBC could accelerate the progression of PCa through regulating miR-1245b-5p/CASK axis, which provided a potential therapeutic target for PCa treatment.
Methods
LncRNA AATBC and miR-1245b-5p expression were evaluated using RT-qPCR. CCK-8, colony-formation, apoptosis and transwell assay were used to analyze the in vitro role. The xenograft model was used to explore the in vivo role. Bioinformatics analysis and a dual luciferase assay, RIP and RNA pull down were used to confirm the interaction between lncRNA AATBC and 1245b-5p, as well as 1245b-5p and CASK.
Results
Firstly, we certified that the expression of AATBC was augmented in PCa, and knockdown of AATBC could significantly inhibit the growth of PCa in vitro and in vivo. Mechanistically, our results manifested that AATBC could directly bind to miR-1245b-5p. In addition, miR-1245b-5p played cancer-suppressive role in PCa cells. Moreover, CASK was attested as the target of miR-1245b-5p, and CASK was demonstrated to exert as oncogene in the progression of PCa. Finally, rescue assays illustrated that miR-1245b-5p downregulation or CASK restoration could greatly resist the restrained effects of AATBC knockdown on PCa progression.