BACKGROUND: Cancer stem cells (CSCs) support colorectal cancer progression and therapy resistance, yet the redox regulators that sustain CSC identity are incompletely defined. We investigated the role of peroxiredoxin 5 (PRX5) in CSC formation and tumorigenicity using HCT116 colorectal cancer models. METHODS: xenograft tumorigenicity in BALB/c-nu mice. RESULTS: , PRX5-overexpressing xenografts grew faster, achieving a 2.5-fold greater tumor volume by day 19 and a 1.82-fold higher mean tumor weight compared with controls. Tumor tissues showed elevated OCT4, SOX2, NANOG, CD133, and EPCAM. CONCLUSION: PRX5 contributes to maintaining a redox environment associated with STAT3 activation and core stemness programs in CRC, promoting CSC phenotypes and tumorigenicity. Targeting PRX5-mediated redox signaling may warrant further investigation as a potential approach to disrupt CSC maintenance and overcome chemoresistance.
Lee et al. (Sat,) studied this question.