Upregulation of cell division cycle 20 in cisplatin resistance-induced epithelial-mesenchymal transition in osteosarcoma cells.

Abstract

Cell division cycle 20 homologue (Cdc20) is characterized as an oncoprotein that is involved in carcinogenesis. Accumulated evidence reveals that Cdc20 plays an oncogenic role by governing cell growth, apoptosis, motility, and metastasis. The role of Cdc20 in drug resistance is elusive. In the present study, we exploited whether Cdc20 is involved in the cisplatin (DDP) resistance-induced epithelial-mesenchymal transition (EMT) of osteosarcoma cells. We found that DDP resistant U2OS and MG63 cells underwent EMT. Moreover, DDP-resistant cells exhibit the mesenchymal features such as enhanced attachment and detachment and increased invasion activity and migration. Mechanistically, Cdc20 was highly expressed in DDP-resistant osteosarcoma cells compared to parental cells. Consistently, downregulation of CdcC20 in DDP-resistant cells reversed the EMT phenotypes and changed the expression of EMT biomarkers. Our studies provide evidence for targeting Cdc20 as a promising approach to enhancing drug sensitivity for the treatment of osteosarcoma.