PURPOSE: It has been proved that miR-505 expression was changed in prostate cancer (PC) tissues. However, its role and molecular mechanism in PC cells remains unclear. Our study aimed to study the microRNA (miR)-505 potential role and potential mechanism in PC cells. METHODS: miR-505 and HMGB-1 expression in PC tissues and cells was measured by RT-PCR and western blot, respectively. MiR-505 mimic or inhibitor was applied to increase or decrease miR-505 expression in DU145 cells separately. Invaded cells and migrated cells were detected by transwell assay. Epithelial-mesenchymal transition (EMT) was evalauted using western blot. Moreover, Luciferase reporter assay was carried out to confirm miR-505's target gene. RESULTS: miR-505 expression was declined while HMGB-1 expression was raised in PC tissues and cells. Furthermore, increasing miR-505 expression suppressed, whereas decreasing miR-505 expression promoted cell invasion, migration and EMT in DU145 cells. Moreover, miR-505 could target HMGB-1 in regulating PC progression. Knockdown of HMGB-1 inhibited cell invasion and migration and re-expression of HMGB-1 reversed miR-505 mimic inhibitory effect on PC cell invasion and migration. CONCLUSION: We conclude that miR-505 suppressed cell invasion, metastasis and ETM through targeting HMGB-1, which provided a potential target for PC treatment.
PURPOSE: It has been proved that miR-505 expression was changed in prostate cancer (PC) tissues. However, its role and molecular mechanism in PC cells remains unclear. Our study aimed to study the microRNA (miR)-505 potential role and potential mechanism in PC cells. METHODS:miR-505 and HMGB-1 expression in PC tissues and cells was measured by RT-PCR and western blot, respectively. MiR-505 mimic or inhibitor was applied to increase or decrease miR-505 expression in DU145 cells separately. Invaded cells and migrated cells were detected by transwell assay. Epithelial-mesenchymal transition (EMT) was evalauted using western blot. Moreover, Luciferase reporter assay was carried out to confirm miR-505's target gene. RESULTS:miR-505 expression was declined while HMGB-1 expression was raised in PC tissues and cells. Furthermore, increasing miR-505 expression suppressed, whereas decreasing miR-505 expression promoted cell invasion, migration and EMT in DU145 cells. Moreover, miR-505 could target HMGB-1 in regulating PC progression. Knockdown of HMGB-1 inhibited cell invasion and migration and re-expression of HMGB-1 reversed miR-505 mimic inhibitory effect on PC cell invasion and migration. CONCLUSION: We conclude that miR-505 suppressed cell invasion, metastasis and ETM through targeting HMGB-1, which provided a potential target for PC treatment.