circSMAD2 governs migration and epithelial-mesenchymal transition by inhibiting microRNA-9.

Epithelial-mesenchymal transition (EMT) culminates the cancer process. Studies found circular RNA-SMAD2 (circSMAD2) impedes EMT by regulating microRNA (miR). Here, we intended to investigate the role of circSMAD2-miR-9 node in prostate cancer cells. Tissue specimens were procured from 20 patients with prostate cancer. LNCaP and PC-3 cells were transfected with the plasmid bearing circSMAD2 or miR-9 mimic. circSMAD2 and miR-9 were quantified by quantitative reverse transcription polymerase chain reaction. The cells were subjected to assays for viability, proliferation, and migration. EMT process was evaluated by investigating the phosphorylation of SMAD2, alteration of cadherin switch, and accumulation of vimentin. STAT and MEK/ERK pathways were then determined by Western blot. We found that the tumor tissues showed a decrement in circSMAD2. Restoration of circSMAD2 inhibited the proliferative and migratory activities, and impaired EMT process of LNCaP and PC-3 cells. Moreover, circSMAD2-overexpressed cells showed a decrease in miR-9. Upregulating miR-9 abolished the inhibitory role of circSMAD2 in proliferation, migration, and EMT. Furthermore, circSMAD2 abated the phosphorylation of STAT3, MEK, and ERK, while miR-9 mimic rehabilitated the phosphorylated expression. In conclusion, miR-9 inhibition is required for circSMAD2 to abate migration and EMT process in prostate cancer cells.