Garg M, Niharika. Ferroptosis, autophagy, and mitochondrial dynamics: Front burners in cancer therapeutics. World J Clin Oncol 2025; 16(11): 113193 [DOI: 10.5306/wjco.v16.i11.113193]
Corresponding Author of This Article
Minal Garg, Full Professor, Department of Biochemistry and Director, Institute of Advanced Molecular Genetics and Infectious Diseases, University of Lucknow, University Road, Lucknow 226007, Uttar Pradesh, India. garg_minal@lkouniv.ac.in
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Oncology
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Editorial
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
Nov 24, 2025 (publication date) through Nov 21, 2025
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Publication Name
World Journal of Clinical Oncology
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2218-4333
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Garg M, Niharika. Ferroptosis, autophagy, and mitochondrial dynamics: Front burners in cancer therapeutics. World J Clin Oncol 2025; 16(11): 113193 [DOI: 10.5306/wjco.v16.i11.113193]
World J Clin Oncol. Nov 24, 2025; 16(11): 113193 Published online Nov 24, 2025. doi: 10.5306/wjco.v16.i11.113193
Ferroptosis, autophagy, and mitochondrial dynamics: Front burners in cancer therapeutics
Minal Garg, Niharika
Minal Garg, Department of Biochemistry and Director, Institute of Advanced Molecular Genetics and Infectious Diseases, University of Lucknow, Lucknow 226007, Uttar Pradesh, India
Niharika, Department of Biochemistry, University of Lucknow, Lucknow 226007, Uttar Pradesh, India
Co-corresponding authors: Minal Garg and Niharika.
Author contributions: Garg M and Niharika contributed to this paper and have agreed with the submission in its present form.
Conflict-of-interest statement: All the authors report 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: Minal Garg, Full Professor, Department of Biochemistry and Director, Institute of Advanced Molecular Genetics and Infectious Diseases, University of Lucknow, University Road, Lucknow 226007, Uttar Pradesh, India. garg_minal@lkouniv.ac.in
Received: August 19, 2025 Revised: August 27, 2025 Accepted: October 21, 2025 Published online: November 24, 2025 Processing time: 94 Days and 20.9 Hours
Abstract
This article comments on the article by Rana and Prajapati published in the recent issue. Cancer remains the most formidable public health problem and contributes to significant mortality worldwide. Tumor heterogeneity, toxicity and acquired resistance limit the efficacy of widely used cancer therapies such as radiotherapy, chemotherapy, gene therapy, and immunotherapy. Regulated cell death maintains cellular homeostasis and is a primary hallmark of cancer. Review by Rana and Prajapati discusses the mechanistic regulation of ferroptosis, autophagy, and mitochondrial dynamics in cancer and highlights the therapeutic possibilities of these regulated cell death pathways for developing more effective and targeted cancer therapies, mainly for aggressive and drug-resistant tumors. Considering the important regulatory role of ferroptosis, autophagy and its dynamic interplay with mitochondrial metabolism in tumor pathogenesis, therapy resistance and metastasis, reshaping of the tumor microenvironment with modulations in autophagy and mitochondrial function could sensitize ferroptosis-resistant tumors to anticancer drugs thereby increase the therapeutic efficacy of existing treatment regimens. Deeper understanding of the crosstalk may lead to the identification of non-invasive biomarkers for detecting ferroptosis-sensitive and resistant tumors, prediction of treatment response and the development of clinically translatable pharmacological strategies to maximize patient benefit while minimizing adverse outcomes.
Core Tip: Considering the important regulatory role of ferroptosis, autophagy and its dynamic interplay with mitochondrial metabolism in tumor pathogenesis, therapy resistance and metastasis, reshaping of the tumor microenvironment with the modulations in autophagy and mitochondrial function could sensitize ferroptosis-resistant tumors to anti-cancer drugs thereby increase the therapeutic efficacy of existing treatment regimens.
