Gupta P, Parveen S, Kumar S, Ahtsham A, Banerjee M. Attack cancer: Through autophagic modulations as suppressor or promoter. World J Clin Oncol 2025; 16(11): 112313 [DOI: 10.5306/wjco.v16.i11.112313]
Corresponding Author of This Article
Saurabh Kumar, PhD, Department of Zoology, Molecular and Human Genetics Laboratory, University of Lucknow, University Road, Babuganj, Lucknow 226007, Uttar Pradesh, India. saurabhdhuriya110@gmail.com
Research Domain of This Article
Oncology
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Review
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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
ISSN
2218-4333
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Gupta P, Parveen S, Kumar S, Ahtsham A, Banerjee M. Attack cancer: Through autophagic modulations as suppressor or promoter. World J Clin Oncol 2025; 16(11): 112313 [DOI: 10.5306/wjco.v16.i11.112313]
World J Clin Oncol. Nov 24, 2025; 16(11): 112313 Published online Nov 24, 2025. doi: 10.5306/wjco.v16.i11.112313
Attack cancer: Through autophagic modulations as suppressor or promoter
Pratishtha Gupta, Shama Parveen, Saurabh Kumar, Ana Ahtsham, Monisha Banerjee
Pratishtha Gupta, Shama Parveen, Saurabh Kumar, Ana Ahtsham, Monisha Banerjee, Department of Zoology, Molecular and Human Genetics Laboratory, University of Lucknow, Lucknow 226007, Uttar Pradesh, India
Co-first authors: Pratishtha Gupta and Shama Parveen.
Co-corresponding authors: Saurabh Kumar and Monisha Banerjee.
Author contributions: Gupta P contributed to designed research, literature search, wrote the paper and figure preparation; Parveen S contributed to literature search, manuscript writing and editing; Kumar S contributed to manuscript writing & editing; Ahtsham A contributed to manuscript writing and figure preparation; Banerjee M contributed to manuscript editing and supervision. all authors have read and approved the final manuscript. It is reasonable to have two co-corresponding authors for this review article because the work covers a wide range of topics and fields. The review brings together different areas of knowledge. One author is in charge of critically putting together experimental and clinical evidence, while the other is in charge of framing the ideas, organizing the material, and making sure that all of the most recent breakthroughs are covered. By sharing the responsibility, both authors can quickly answer questions from readers, reviewers, and editors, depending on the subject or technical background of the question. This shared accountability recognizes their equal intellectual contributions, guarantees accuracy across disciplines, and underscores the collaborative essence of the review process.
Supported by DBT-BUILDER-University of Lucknow Interdisciplinary Life Science Programme for Advance Research and Education (Level II), No. TG BT/INF/22/SP47623/2022.
Conflict-of-interest statement: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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: Saurabh Kumar, PhD, Department of Zoology, Molecular and Human Genetics Laboratory, University of Lucknow, University Road, Babuganj, Lucknow 226007, Uttar Pradesh, India. saurabhdhuriya110@gmail.com
Received: July 25, 2025 Revised: August 14, 2025 Accepted: October 28, 2025 Published online: November 24, 2025 Processing time: 121 Days and 12 Hours
Abstract
Organelle integrity and maintenance of protein homeostasis and purpose is essential for fundamental equilibrium and survivability. Autophagy is the primary process which regulates the distribution of different cell loads to lysosomes for destruction and reuse. Extensive research illustrates the protective functions of autophagy against various diseases. Though in cancer, noticeably contrasting functions of autophagy have been evaluated in the prohibition of preliminary tumor evolution vs the continuance and, anabolic and catabolic variations of well-established and invasive tumors. Autophagy possesses numerous roles in tumor microenvironment (TME) establishment and associated immune cells function which is addressed in recent studies. Autophagic machinery which is employed in different autophagy-related pathways contributes to metastatic diseases and are distinct from classical autophagy. Therapeutic strategies based on the inhibition or induction of autophagy and related processes has helped in the designing of efficient anticancer drugs. According to the review, we evaluate and decipher the various purposes of autophagy and its association with autophagy mechanisms in course of tumor development, invasion and progression. We summarize the latest findings involving the role of these activities including tumor cells and TME and define further breakthrough in therapy aiming at autophagic activities in cancer.
Core Tip: Autophagy plays a crucial role in the breakdown and recycling of cellular components. However, its role in cancer biology is complex and multifaceted. It can inhibit or help tumor growth depending on cancer type, stage, and situation. Autophagy helps cancer cells withstand environmental stress, such as lack of oxygen, nutrients, or chemotherapy. Recent studies have shown that autophagy signaling pathways are complicated and can be changed to treat it. Stopping autophagy may improve the sensitivity of cancer cells to chemotherapy. Increasing autophagy can kill cancer cells, especially apoptosis-resistant ones. Thus, autophagy targeting is a promising but difficult cancer treatment.