lncRNA ADAMTS9-AS1 promotes bladder cancer cell invasion, migration, and inhibits apoptosis and autophagy through PI3K/AKT/mTOR signaling pathway

Bladder cancer is the most common cancer in the urinary system which has threatened lives. Increasing evidence has shown that lncRNAs were expressed in cancer cells as a biomarker and might regulate cancer cell development and progression. It was reported that ADAMTS9-AS1 plays a suppressive role in tumor cell growth and proliferation in prostate cancer. However, it remains unclear whether ADAMTS9-AS1 influences the function of bladder cancer cells. In this study, we detected that ADAMTS9-AS1 is highly expressed in bladder cancer. We observed that the up-regulation of ADAMTS9-AS1 promoted cell proliferation, migration and invasion, and reduced the apoptosis and autophagy of 5637 and T42 cell lines. Meanwhile, the down-regulation of ADAMTS9AS1 increased the apoptosis and autophagy, and suppressed their proliferation, migration and invasion. Interestingly, the up-regulation of ADAMTS9-AS1 was accompanied by the activation of PI3K/AKT/mTOR signaling pathway, while the down-regulation of ADAMTS9-AS1 lead to an opposite effect. Together, these results demonstrated that ADAMTS9-AS1 promotes bladder cancer cell invasion and migration, and negatively regulates bladder cancer cell apoptosis and autophagy, which might be through PI3K/AKT/mTOR signaling pathway. Targeting ADAMTS9-AS1 might become a potential therapeutic approach in treating bladder cancer.

Automated summary

The study revealed that the high expression of ADAMTS9-AS1 in bladder cancer promotes cell proliferation, migration, and invasion while reducing apoptosis and autophagy. It was also observed that ADAMTS9-AS1 may regulate these processes through the PI3K/AKT/mTOR signaling pathway. Targeting ADAMTS9-AS1 could be a potential therapeutic approach for treating bladder cancer.