Overexpression of peroxiredoxin 2 inhibits TGF-β1-induced epithelial-mesenchymal transition and cell migration in colorectal cancer.

Although human peroxiredoxin 2 (PRDX2) has been implicated in tumor progression (e.g., invasion and metastasis), little is known regarding its role in the epithelial‑mesenchymal transition (EMT) process during tumorigenesis. The present study offers the first evidence, to the best of our knowledge, that the antioxidant enzyme PRDX2 has an important role in regulating the EMT process. It was demonstrated that overexpression of PRDX2 leads to changes in cell morphology in vitro and potent inhibition of the transforming growth factor (TGF)‑β1‑induced EMT and cell migration of colorectal cancer (CRC) cells. Furthermore, PRDX2 regulates the expression of EMT markers, EMT‑related transcription factors and metastasis‑related factors in CRC cells. These results provide new insight into the role of PRDX2 in regulating EMT, cell migration and metastasis of CRC cells. It was concluded that the upregulation of PRDX2 may be correlated with EMT and contributes to the pathogenesis of CRC by inhibiting EMT, cell migration and metastasis. Taken together, these findings suggest that PRDX2 may be a key regulator of invasion and metastasis by inhibiting EMT of CRC cells, and also identifies a therapeutic strategy to effectively decrease the lethality of highly malignant types of CRC.