Editorial Open Access
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
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, 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
ORCID number: Nabil Eid (0000-0002-2938-2618).
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.

Key Words: Colon cancer; Human β-defensin-1; Long noncoding RNA; Mammalian target of rapamycin; Autophagy; LC3-II; Beclin-1; Autophagy flux

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.
INTRODUCTION

Autophagy is a prosurvival mechanism for clearing and recycling damaged cellular components, specifically upregulated upon exposure to various stressors such as oxidative stress, misfolded proteins, organelle damage, hypoxia, and cancer chemotherapy. Autophagy is tightly controlled, and AuTophaGy-related (ATG) proteins play a key role. To date, more than 41 ATG genes have been identified. Mechanistically, autophagy is stimulated by suppression of the mammalian target of rapamycin (mTOR), resulting in the formation of Beclin-1-mediated autophagosomal membranes, which sequester cellular components forming LC3 II-regulated autophagosomes. Autolysosomes are then formed by the fusion of autophagosomes with lysosomes via LAMP-2 and cleared by lysosomal cathepsins[1-4].

HUMAN Β-DEFENSIN INHIBITS MTOR, AND UPREGULATES AUTOPHAGY MARKERS IN COLON CANCER CELLS

An interesting study by Zhao et al[5] found that human β-defensin-1 (hBD-1) reduced the proliferation of SW620 human colon cancer cells, which was associated with the inhibition of the mTOR, resulting in autophagy activation. The activation of autophagy is evidenced by increased expression of Beclin1 and LC3II/I protein levels using the Western blot method. It has been reported that mTOR inhibition and AMPK activation regulate autophagy through the direct phosphorylation of Ulk1[6-8]. The reduced proliferation of colon cancer cells by hBD-1 is consistent with its tumor suppressor effects, such as the induction of apoptosis and inhibition of metastasis in various types of cancers[5,9,10]. However, a few questions related to Zhao’s study need to be answered. Is the increase in LC3-II an indication of increased autophagic flux? How does autophagy activation affect colon cancer cells? Does it function as a mechanism for survival?

The answer to the first question is that upregulation of LC3-II (autophagosome marker) indicates autophagy activation and the formation of autophagosomes; however, it is not an indicator of the autophagic flux per se, but may reflect autophagosome accumulation, which results from the fusion failure of autophagosomes with lysosomes or lysosomal dysfunction (incomplete autophagy). Autophagic flux (a measure of autophagic degradation activity and complete autophagy) can be measured using lysosomal inhibitors such as chloroquine[1,2].

The answer to the second question is that autophagy activation in cancer cells could be a prosurvival or pro-death mechanism. To prove these possibilities (answer of third question), hBD-1-treated cancer cells[5] should be exposed to either 3-methyladenine, an inhibitor of early autophagosome formation[11] or lysosomal inhibitors[1,2]. Reduction of cancer cell viability upon autophagy inhibition indicates the prosurvival role of autophagy. Therefore, autophagy inhibition in cancer cells could enhance the tumor suppressing effect of hBD-1[1].

On the other hand, if the viability of cancer cells is enhanced after autophagy blocking, this indicates that autophagy is a pro-death mechanism or has no effect on cancer cell viability (bystander effect)[1,2,11].

MODULATION OF AUTOPHAGY BY LONG NONCODING RNAS IN SW620 COLON CANCER CELLS

A growing body of evidence indicates that long noncoding RNAs (lncRNAs) are expressed in most cancers with autophagy-modulating roles, impacting the survival of several cancers[12,13]. In their study[5], the authors found that hBD1-treated SW620 colon cancer cells exhibited upregulated expression of lncRNA TCONS_00014506. Inhibition of the lncRNA TCONS_00014506 resulted in increased p-mTOR expression, and decreased Beclin1 and LC3 II protein levels, reversing the pro-autophagic effects of hBD1 on cancer cells. This indicates that hBD-1 inhibits p-mTOR expression and promotes autophagy in SW620 cells via the regulation of lncRNA TCONS_00014506 expression.

We believe that providing a more detailed explanation of the process for the selection of lncRNAs in the study of Zhao et al[5] would greatly benefit the scientific community and enhance the overall clarity of the paper. The selection process of long non-coding RNAs is a crucial aspect of the study, and a comprehensive explanation would contribute significantly to the readers’ understanding and appreciation of the research. Including information on the criteria used for selection, the rationale behind those criteria, and any experimental validations performed to confirm the selection would provide valuable insights. This transparency will not only aid in the interpretation of the findings but also contribute to the reproducibility of the study by allowing other researchers to replicate and validate the results. We feel that the authors could have considered expanding the relevant section in the manuscript to include a more thorough description of the long non-coding RNA selection process. This addition will undoubtedly improve the manuscript’s clarity and contribute to its overall impact in the scientific community. Importantly, we advise the authors to check the quality of their figures as some figures are not clear and incomplete. A schematic Figure 1 depicting the summary of the results and conclusions of this study is provided below.

Figure 1
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Figure 1 Human β-defensin-1-induced inhibition of the mammalian target of rapamycin in human colon cancer and autophagy activation via long non-coding RNA TCONS_0014506. Human β-defensin-1 (hBD1)-treated cancer cells exhibit proliferation suppression, autophagy activation, and upregulation of long non-coding RNA TCONS_00014506. Genetic Inhibition of this RNA reverses the enhanced autophagic response by hBD1. However, the role of autophagy activation in cancer cells by treatment needs further studies. hBD1: Human β-defensin-1; mTOR: Mammalian target of rapamycin; LncRNA: Long non-coding RNA.
CONCLUSION

In conclusion, hBD-1-induced activation of autophagy in SW620 colon cancer cells is mediated by the suppression of p-mTOR and upregulation of lncRNA TCONS00014506. Further research is needed to explore the modulating effects of lncRNAs on autophagy pathways. LncRNAs in cancer cells could serve as prognostic and diagnostic biomarkers, assisting in tumor therapy.

ACKNOWLEDGEMENTS

We would like to thank Prof. James Edward Walsh, MSc, PhD (IMU University) for the English editing of this manuscript.

Footnotes

Provenance and peer review: Invited article; Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Cell biology

Country of origin: Malaysia

Peer-review report’s classification

Scientific Quality: Grade B

Novelty: Grade B

Creativity or Innovation: Grade B

Scientific Significance: Grade B

P-Reviewer: Guo D, China S-Editor: Chen YL L-Editor: A P-Editor: Zhao YQ

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