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

Int J Biochem Cell Biol. 2021 Nov:140:106069. doi: 10.1016/j.biocel.2021.106069. Epub 2021 Aug 21.

Abstract

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 ADAMTS9-AS1 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.

Keywords: ADAMTS9-AS1; Apoptosis and autophagy; Bladder cancer; PI3K/AKT/mTOR signaling pathway.

MeSH terms

  • Apoptosis
  • Autophagy
  • Cell Proliferation
  • Phosphatidylinositol 3-Kinases*
  • Proto-Oncogene Proteins c-akt*
  • RNA, Long Noncoding
  • Signal Transduction
  • Urinary Bladder Neoplasms

Substances

  • RNA, Long Noncoding
  • Proto-Oncogene Proteins c-akt