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Antioxidants
Special Issues
Redox-Modulating Strategies in Cancer Therapy: Targeted Thioredoxin System Inhibition
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Redox-Modulating Strategies in Cancer Therapy: Targeted Thioredoxin System Inhibition

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Antioxidant Enzyme Systems".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 2828

Special Issue Editor

Prof. Dr. Jianguo Fang

E-Mail Website
Guest Editor
School of Chemistry and Chemical Engineering, Nanjing University of Science and Technology (NJUST), Nanjing 210094, China
Interests: redox regulation; reactive oxygen species; thioredoxin; fluorescent probes; anticancer agent
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The mammalian thioredoxin system, including the core components thioredoxins and thioredoxin reductases as well as the related downstream proteins (e.g., the peroxiredoxins and the methionine sulfoxide reductases), play a crucial role in maintaining cellular redox homeostasis and regulating diverse signaling pathways. Tumor cells harbor a different redox microenvironment from that of noncancer cells, and this redox microenvironment is pivotal for tumor initiation, proliferation and metastasis. Thus, interfering with redox signaling in cancer cells has been recognized as an emerging strategy for cancer therapy.

This Special Issue entitled “Redox-Modulating Strategies in Cancer Therapy: Targeted Thioredoxin System Inhibition” aims to report the latest progress in cancer therapy made via inhibiting the thioredoxin system. All relevant studies are welcome. The Special Issue will include but not be limited to the following topics:

  • Novel small molecules targeting the thioredoxin system for cancer therapy;
  • Novel approaches targeting the thioredoxin system for cancer therapy;
  • Novel action mechanisms of redox-interfering molecules;
  • Novel redox-dependent signaling pathways in cancer cells;
  • The clinical development of thioredoxin system inhibitors;
  • Review/commenting articles related to the topic.

Prof. Dr. Jianguo Fang
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

  • redox
  • cancer
  • thioredoxin
  • peroxiredoxin
  • reactive oxygen species

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Published Papers (3 papers)

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Research

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17 pages, 6413 KiB  
Article
Bufotalin Induces Oxidative Stress-Mediated Apoptosis by Blocking the ITGB4/FAK/ERK Pathway in Glioblastoma
by Junchao Tan, Guoqiang Lin, Rui Zhang, Yuting Wen, Chunying Luo, Ran Wang, Feiyun Wang, Shoujiao Peng and Jiange Zhang
Antioxidants 2024, 13(10), 1179; https://doi.org/10.3390/antiox13101179 - 27 Sep 2024
Viewed by 660
Abstract
Bufotalin (BT), a major active constituent of Chansu, has been found to possess multiple pharmacological activities. Although previous studies have shown that BT could inhibit the growth of glioblastoma (GBM), the safety of BT in vivo and the potential mechanism are still unclear. [...] Read more.
Bufotalin (BT), a major active constituent of Chansu, has been found to possess multiple pharmacological activities. Although previous studies have shown that BT could inhibit the growth of glioblastoma (GBM), the safety of BT in vivo and the potential mechanism are still unclear. We conducted a systematic assessment to investigate the impact of BT on GBM cell viability, migration, invasion, and colony formation. Furthermore, in vivo results were obtained to evaluate the effect of BT on tumor growth. The preliminary findings of our study demonstrate the effective inhibition of GBM cell growth and subcutaneous tumor development in mice by BT, with tolerable levels of tolerance observed. Mechanistically, BT treatment induced mitochondrial dysfunction, bursts of reactive oxygen species (ROS), and subsequent cell apoptosis. More importantly, proteomic-based differentially expressed proteins analysis revealed a significant downregulation of integrin β4 (ITGB4) following BT treatment. Furthermore, our evidence suggested that the ITGB4/focal adhesion kinase (FAK)/extracellular signal-related kinase (ERK) pathway involved BT-induced apoptosis. Overall, our study demonstrates the anti-GBM effects of BT and elucidates the underlying mechanism, highlighting BT as a potential therapeutic option for GBM. Full article
(This article belongs to the Special Issue Redox-Modulating Strategies in Cancer Therapy: Targeted Thioredoxin System Inhibition)
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Review

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15 pages, 1382 KiB  
Review
Glutathione Peroxidases: An Emerging and Promising Therapeutic Target for Pancreatic Cancer Treatment
by Paula Iglesias-Matesanz, Carlos Lacalle-Gonzalez, Carlos Lopez-Blazquez, Michael Ochieng’ Otieno, Jesus Garcia-Foncillas and Javier Martinez-Useros
Antioxidants 2024, 13(11), 1405; https://doi.org/10.3390/antiox13111405 - 16 Nov 2024
Viewed by 488
Abstract
Glutathione peroxidases (GPxs) are a family of enzymes that play a critical role in cellular redox homeostasis through the reduction of lipid hydroperoxides to alcohols, using glutathione as a substrate. Among them, GPx4 is particularly of interest in the regulation of ferroptosis, a [...] Read more.
Glutathione peroxidases (GPxs) are a family of enzymes that play a critical role in cellular redox homeostasis through the reduction of lipid hydroperoxides to alcohols, using glutathione as a substrate. Among them, GPx4 is particularly of interest in the regulation of ferroptosis, a form of iron-dependent programmed cell death driven by the accumulation of lipid peroxides in the endoplasmic reticulum, mitochondria, and plasma membrane. Ferroptosis has emerged as a crucial pathway in the context of cancer, particularly pancreatic cancer, which is notoriously resistant to conventional therapies. GPx4 acts as a key inhibitor of ferroptosis by detoxifying lipid peroxides, thereby preventing cell death. However, this protective mechanism also enables cancer cells to survive under oxidative stress, which makes GPx4 a potential druggable target in cancer therapy. The inhibition of GPx4 can trigger ferroptosis selectively in cancer cells, especially in those that rely heavily on this pathway for survival, such as pancreatic cancer cells. Consequently, targeting GPx4 and other GPX family members offers a promising therapeutic strategy to sensitize pancreatic cancer cells to ferroptosis, potentially overcoming resistance to current treatments and improving patient outcomes. Current research is focusing on the development of small-molecule inhibitors of GPx4 as potential candidates for pancreatic cancer treatment. Full article
(This article belongs to the Special Issue Redox-Modulating Strategies in Cancer Therapy: Targeted Thioredoxin System Inhibition)
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23 pages, 2879 KiB  
Review
Exploring the Thioredoxin System as a Therapeutic Target in Cancer: Mechanisms and Implications
by Rebecca Seitz, Deniz Tümen, Claudia Kunst, Phillip Heumann, Stephan Schmid, Arne Kandulski, Martina Müller and Karsten Gülow
Antioxidants 2024, 13(9), 1078; https://doi.org/10.3390/antiox13091078 - 4 Sep 2024
Cited by 2 | Viewed by 1254
Abstract
Cells constantly face the challenge of managing oxidants. In aerobic organisms, oxygen (O2) is used for energy production, generating reactive oxygen species (ROS) as byproducts of enzymatic reactions. To protect against oxidative damage, cells possess an intricate system of redox scavengers [...] Read more.
Cells constantly face the challenge of managing oxidants. In aerobic organisms, oxygen (O2) is used for energy production, generating reactive oxygen species (ROS) as byproducts of enzymatic reactions. To protect against oxidative damage, cells possess an intricate system of redox scavengers and antioxidant enzymes, collectively forming the antioxidant defense system. This system maintains the redox equilibrium and enables the generation of localized oxidative signals that regulate essential cellular functions. One key component of this defense is the thioredoxin (Trx) system, which includes Trx, thioredoxin reductase (TrxR), and NADPH. The Trx system reverses oxidation of macromolecules and indirectly neutralizes ROS via peroxiredoxin (Prx). This dual function protects cells from damage accumulation and supports physiological cell signaling. However, the Trx system also shields tumors from oxidative damage, aiding their survival. Due to elevated ROS levels from their metabolism, tumors often rely on the Trx system. In addition, the Trx system regulates critical pathways such as proliferation and neoangiogenesis, which tumors exploit to enhance growth and optimize nutrient and oxygen supply. Consequently, the Trx system is a potential target for cancer therapy. The challenge lies in selectively targeting malignant cells without disrupting the redox equilibrium in healthy cells. The aim of this review article is threefold: first, to elucidate the function of the Trx system; second, to discuss the Trx system as a potential target for cancer therapies; and third, to present the possibilities for inhibiting key components of the Trx system, along with an overview of the latest clinical studies on these inhibitors. Full article
(This article belongs to the Special Issue Redox-Modulating Strategies in Cancer Therapy: Targeted Thioredoxin System Inhibition)
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