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©The Author(s) 2026. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 7, 2026; 32(1): 114184
Published online Jan 7, 2026. doi: 10.3748/wjg.v32.i1.114184
Published online Jan 7, 2026. doi: 10.3748/wjg.v32.i1.114184
Peroxiredoxin 1, pyroptosis, and the emerging frontier in colorectal cancer therapy
Dharmendra Kumar Maurya, Radiation Biology & Health Sciences Division, Bhabha Atomic Research Centre, Mumbai 400085, Maharashtra, India
Author contributions: Maurya DK has done review of literature and wrote the editorial.
Conflict-of-interest statement: The author reports no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Dharmendra Kumar Maurya, PhD, Associate professor, Radiation Biology & Health Sciences Division, Bhabha Atomic Research Centre, 3-82-S, A-Block, Modular Laboratory, Mumbai 400085, Maharashtra, India. dkmaurya@barc.gov.in
Received: September 15, 2025
Revised: October 22, 2025
Accepted: November 21, 2025
Published online: January 7, 2026
Processing time: 114 Days and 10.8 Hours
Revised: October 22, 2025
Accepted: November 21, 2025
Published online: January 7, 2026
Processing time: 114 Days and 10.8 Hours
Core Tip
Core Tip: Peroxiredoxin 1, long regarded as an intracellular antioxidant that protect tumors from oxidative stress, assumes a paradoxical role in colorectal cancer therapy. He et al reveal that extracellular peroxiredoxin 1 acts as a damage-associated molecular pattern, activating the NOD-, LRR- and pyrin domain-containing protein 3 inflammasome/caspase-1/gasdermin D pathway to trigger pyroptosis. This lytic, pro-inflammatory death suppresses colorectal cancer proliferation, invasion, and migration while amplifying interleukin-1β/interleukin-18-mediated immune surveillance. Using patient cohorts, recombinant protein assays, and xenograft models, the study rigorously validates this mechanism.