BPG is committed to discovery and dissemination of knowledge
Letter to the Editor
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Nov 28, 2025; 31(44): 114404
Published online Nov 28, 2025. doi: 10.3748/wjg.v31.i44.114404
Peroxiredoxin 1 inhibits tumorigenesis by activating the NLR family pyrin domain containing 3/gasdermin D pathway: Advanced therapies targeting heterogeneous cell death mechanisms
Anna Smirnova, Daria Eygel, Irina Kondrasheva, Denis S Baranovskii, Ilya D Klabukov
Anna Smirnova, Daria Eygel, Irina Kondrasheva, Denis S Baranovskii, Ilya D Klabukov, Department of Regenerative Medicine, National Medical Research Radiological Center of the Ministry of Health of the Russian Federation, Obninsk 249036, Russia
Anna Smirnova, Ilya D Klabukov, Obninsk Institute for Nuclear Power Engineering of the National Research Nuclear University MEPhI, Obninsk 249033, Russia
Irina Kondrasheva, Department of Regenerative Dentistry, Tsiolkovsky Kaluga State University, Kaluga 248023, Russia
Denis S Baranovskii, Institute of Systems Biology and Medicine, Russian University of Medicine, Moscow 127006, Russia
Author contributions: Klabukov ID designed and performed the research, and wrote the letter; Baranovskii DS analyzed the data; Smirnova A, Kondrasheva I, and Eygel D revised the letter.
Supported by Russian Science Foundation, No. 24-64-00028.
Conflict-of-interest statement: There are no conflicts of interest to report.
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: Ilya D Klabukov, PhD, Director, Department of Regenerative Medicine, National Medical Research Radiological Center of the Ministry of Health of the Russian Federation, No. 4 Koroleva Street, Obninsk 249036, Russia. ilya.klabukov@gmail.com
Received: September 18, 2025
Revised: September 30, 2025
Accepted: October 22, 2025
Published online: November 28, 2025
Processing time: 71 Days and 12.5 Hours
Abstract

We read with great interest the advanced research article by He et al, which reported a marked upregulation of peroxiredoxin 1 mRNA and protein levels in colorectal cancer tissues. A central finding of this study was the demonstration of distinct heterogeneity in cell death mechanisms between normal and malignant cells. Current evidence indicates the existence of at least 12 subtypes of programmed cell death, each characterized by unique molecular signatures. The findings of this study have the potential to advance the development of personalized therapies that target cancer cells, representing a promising step forward in cancer treatment. Further advances in targeted mRNA therapy could be achieved by selectively shifting the regulation of cancer cells toward specific pathways of cellular death.

Keywords: Cancer; Cell death; Colorectal cancer; Extracellular matrix; Mechanotransduction; mRNA therapy; Programmed cell death; Pyroptosis; Tumor microenvironment

Core Tip: The molecular patterns of the special types of programmed cell death, such as apoptosis, pyroptosis, ferroptosis, and necroptosis, in cancer cells caused by altered regulation, could improve the effectiveness of mRNA vaccines and targeted therapies by overcoming the barrier function of the tumor microenvironment. Activation of specific pathways to overcome the barrier function in cancer treatment represents a promising strategy for targeted cellular and gene therapies, and also enhances radiosensitivity in radiation therapy.