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8.8
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Journals
Antioxidants
Special Issues
Redox Balance and Autophagy
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Redox Balance and Autophagy

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (15 December 2021) | Viewed by 6232

Special Issue Editor

Dr. Dongmin Kang

E-Mail Website
Guest Editor
Ewha Womans Universitydisabled, Seoul 03760, Korea
Interests: redox signaling; tumor metastasis; cell imaging; phosphoinositide signaling

Special Issue Information

Dear Colleagues,

Autophagy is an essential and defensive cellular degradation program required for cell survival and metabolic homeostasis in response to various stresses, including oxidative stress. The accumulation of damaged organelles, such as fragmented mitochondria, elicits an increase in the cellular level of reactive oxygen species and, thereby, induces autophagy to maintain redox homeostasis. The induced autophagy ameliorates oxidative stress by degrading not only various malfunctioning organelles—including damaged mitochondria, damaged endoplasmic reticulum, and damaged lysosomes—but also damaged macromolecules. Autophagy is critical for survival in cells subjected to oxidative stress. The inhibition of autophagy by chemical regulators or the deletion or knockdown of autophagy-related genes results in apoptotic cell death via disrupting the redox balance. In general, cancer cells exhibit increased autophagy, to manage oxidative stress. Therefore, the use of autophagy inhibitors for cancer treatment has been intensively investigated in animal models and clinical trials.

The contributions to this issue will include the investigation of the molecular mechanisms by which autophagy restores redox balance; the regulation of autophagy; and the roles of autophagy in diseases related to redox stress such as cancer, inflammation and neurodegenerative diseases. Review articles summarizing the current understanding of the role of autophagy in redox homeostasis are welcome.

Dr. Dongmin Kang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Autophagy
  • Reactive oxygen species
  • Redox stress
  • Redox homeostasis
  • Cellular organelle homeostasis
  • Autophagy regulator
  • Redox-stress-related diseases.

Published Papers (1 paper)

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Research

20 pages, 3584 KiB  
Article
Diclofenac: A Nonsteroidal Anti-Inflammatory Drug Inducing Cancer Cell Death by Inhibiting Microtubule Polymerization and Autophagy Flux
by Soohee Choi, Suree Kim, Jiyoung Park, Seung Eun Lee, Chaewon Kim and Dongmin Kang
Antioxidants 2022, 11(5), 1009; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11051009 - 20 May 2022
Cited by 11 | Viewed by 5774
Abstract
Diclofenac, a nonsteroidal anti-inflammatory drug (NSAID) used to treat inflammatory diseases induces cellular toxicity by increasing the production of reactive oxygen species (ROS) and impairing autophagic flux. In this study, we investigated whether diclofenac induces cancer cell death and the mechanism by which [...] Read more.
Diclofenac, a nonsteroidal anti-inflammatory drug (NSAID) used to treat inflammatory diseases induces cellular toxicity by increasing the production of reactive oxygen species (ROS) and impairing autophagic flux. In this study, we investigated whether diclofenac induces cancer cell death and the mechanism by which diclofenac causes cell death. We observed that diclofenac induces mitotic arrest with a half-maximal effective concentration of 170 μM and cell death with a half-maximal lethal dose of 200 µM during 18-h incubation in HeLa cells. Cellular microtubule imaging and in vitro tubulin polymerization assays demonstrated that treatment with diclofenac elicits microtubule destabilization. Autophagy relies on microtubule-mediated transport and the fusion of autophagic vesicles. We observed that diclofenac inhibits both phagophore movement, an early step of autophagy, and the fusion of autophagosomes and lysosomes, a late step of autophagy. Diclofenac also induces the fragmentation of mitochondria and the Golgi during cell death. We found that diclofenac induces cell death further in combination with 5-fuorouracil, a DNA replication inhibitor than in single treatment in cancer cells. Pancreatic cancer cells, which have high basal autophagy, are particularly sensitive to cell death by diclofenac. Our study suggests that microtubule destabilization by diclofenac induces cancer cell death via compromised spindle assembly checkpoints and increased ROS through impaired autophagy flux. Diclofenac may be a candidate therapeutic drug in certain type of cancers by inhibiting microtubule-mediated cellular events in combination with clinically utilized nucleoside metabolic inhibitors, including 5-fluorouracil, to block cancer cell proliferation. Full article
(This article belongs to the Special Issue Redox Balance and Autophagy)
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