Abstract:
: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.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Lu W,Fu Z,Wang H,Feng J,Wei J,Guo Jdoi
10.1016/j.canlet.2013.10.002subject
Has Abstractpub_date
2014-02-28 00:00:00pages
190-9issue
2eissn
0304-3835issn
1872-7980pii
S0304-3835(13)00713-1journal_volume
343pub_type
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