Two patients with KRAS-mutated CRC showed the same mutation in PPL in the same specimen (one serrated change NOS and one TSA with high-grade dysplasia).
These results suggest that Prx2 is an important component in tumoral radiation response, and their inhibition could improve radio and chemoradiotherapy protocols in patients with CRC.
Immunohistochemistry and CD34/periodic acid Schiff double staining were performed to explore the expression of Prdx2 and VM formation in 70 CRC tissues, and there was a positive correlation between Prdx2 expression and VM formation by the Pearson correlation coefficient (r = 0.282, p < 0.05).
In addition, the LoVo CRC cell line was significantly more resistant to hydrogen peroxide (H₂O₂)-induced apoptosis because of a failure to activate pro-apoptotic pathways in contrast to Prdx2 knockdown cells.
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.