Eid N, Davamani F. Human β-defensin-1 activates autophagy in human colon cancer cells via regulation of long non-coding RNA TCONS_00014506. World J Gastrointest Oncol 2024; 16(7): 2894-2901 [DOI: 10.4251/wjgo.v16.i7.2894]
Corresponding Author of This Article
Nabil Eid, Doctor, MD, PhD, Academic Editor, Associate Professor, Senior Lecturer, Senior Scientist, Anatomy Department, Division of Human Biology, School of Medicine, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia. nabilsaleheid@imu.edu.my
Research Domain of This Article
Cell Biology
Article-Type of This Article
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/
World J Gastrointest Oncol. Jul 15, 2024; 16(7): 2894-2901 Published online Jul 15, 2024. doi: 10.4251/wjgo.v16.i7.2894
Human β-defensin-1 activates autophagy in human colon cancer cells via regulation of long non-coding RNA TCONS_00014506
Nabil Eid, Fabian Davamani
Nabil Eid, Anatomy Department, Division of Human Biology, School of Medicine, International Medical University, Kuala Lumpur 57000, Malaysia
Fabian Davamani, Division of Applied Biomedical Sciences and Biotechnology, School of Health Sciences, International Medical University, Kuala Lumpur 57000, Malaysia
Author contributions: Eid N and Davamani F wrote and revised the manuscript; and all authors read and approved the final draft.
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: Nabil Eid, Doctor, MD, PhD, Academic Editor, Associate Professor, Senior Lecturer, Senior Scientist, Anatomy Department, Division of Human Biology, School of Medicine, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia. nabilsaleheid@imu.edu.my
Received: March 7, 2024 Revised: April 26, 2024 Accepted: May 14, 2024 Published online: July 15, 2024 Processing time: 127 Days and 0.1 Hours
Abstract
Macroautophagy (hereafter referred to as autophagy) is a prosurvival mechanism for the clearance of damaged cellular components, specifically related to exposure to various stressors such as starvation, excessive ethanol intake, and chemotherapy. This editorial reviews and comments on an article by Zhao et al, to be published in World J Gastrointestinal Oncology in 2024. Based on various molecular biology methodologies, they found that human β-defensin-1 reduced the proliferation of colon cancer cells, which was associated with the inhibition of the mammalian target of rapamycin, resulting in autophagy activation. The activation of autophagy is evidenced by increased levels of Beclin1 and LC3II/I proteins and mediated by the upregulation of long non-coding RNA TCONS_00014506. Our study discusses the impact of autophagy activation and mechanisms of autophagy, including autophagic flux, on cancer cells. Additionally, we emphasize the importance of describing the detailed methods for isolating long noncoding RNAs TCONS_00014506. Our review will benefit the scientific community and improve the overall clarity of the paper.
Core Tip: Autophagy is an essential mechanism for clearing harmful cellular components, specifically upon exposure to various stressors such as chemotherapy. The activation of autophagy in colon cancer cells under human β-defensin-1 treatment is mediated by mammalian target of rapamycin suppression and upregulation of long noncoding RNAs (lncRNA) TCONS_00014506. Targeting this lncRNA could have prognostic, diagnostic, and therapeutic implications in colon cancer.
