Suppression of STIM1 inhibits the migration and invasion of human prostate cancer cells and is associated with PI3K/Akt signaling inactivation.

Abstract

Store-operated calcium entry (SOCE) plays an important role in the invasion and migration of cancer cells. Stromal-interacting molecule 1 (STIM1) is a critical component in the SOCE. STIM1 has been attracting more and more attention due to its oncogenic potential. STIM1 inhibition suppresses cell proliferation, migration and invasion in a variety of cancer models both in vitro and in vivo. However, the role of STIM1 in prostate carcinogenesis, in particular, in tumor migration and invasion is unclear. Herein, we downregulated STIM1 in prostate cancer cells by lentivirus-mediated short hairpin (shRNA), and then studied its impacts on cell migration and invasion. We found that migration and invasion of prostate cancer cells were significantly inhibited after the suppression of STIM1. Furthermore, we demonstrated that the PI3K/Akt signaling pathway was inactivated by STIM1 knockdown. The PI3K inhibitor LY294002 synergized with STIM1 knockdown to inhibit cell motility. Our results revealed that STIM1 may act as a novel regulator to promote migration and invasion of prostate cancer cells and is associated with the activation of the PI3K/Akt signaling pathway.