Peroxiredoxin 2 knockdown by RNA interference inhibits the growth of colorectal cancer cells by downregulating Wnt/β-catenin signaling

Peroxiredoxin 2 (Prdx2) has been shown to act as an antioxidant whose main function is to reduce hydrogen peroxide (H2O2) in cells, and Prdx2 is abnormally elevated in colorectal cancer (CRC). However, the functional significance of this up-regulation and the detailed molecular mechanism behind the regulatory effect of Prdx2 on the growth of CRC cells have not been elucidated. In this study, we demonstrated that Prdx2 knockdown using a lentiviral vector-mediated specific shRNA inhibited cell growth, stimulated apoptosis, and augmented the production of endogenous reactive oxygen species (ROS). Further, silencing of Prdx2 resulted in an altered expression of proteins associated with the Wnt signaling pathway. Finally, Prdx2 knockdown contributed to attenuated CRC growth in BALB/c nude mice. In conclusion, these findings demonstrate that the regulatory effects of Prdx2 can be partially attributed to Wnt/β-catenin signaling.