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NRF2/KEAP1 Signalling in Cancer
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NRF2/KEAP1 Signalling in Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 July 2025 | Viewed by 4456

Special Issue Editor

Dr. Sonia Fantone

E-Mail Website
Guest Editor
Department of Experimental and Clinical Medicine, Università Politecnica delle Marche, 60126 Ancona, Italy
Interests: oxidative stress; cancer; aging; senescence; inflammation; ovarian cancer; prostate cancer; antioxidants

Special Issue Information

Dear Colleagues,

We are pleased to invite you to submit a manuscript to the Special Issue “NRF2/KEAP1 Signalling in Cancer”. The nuclear factor erythroid 2-related factor 2 (NRF2)/Kelch-like ECH-associated protein 1 (KEAP1) is the most studied signaling pathway involved in cellular defense against oxidative stress, a process characterized by an imbalance between the production of reactive oxygen species (ROS) and antioxidant defenses. Oxidative stress is considered a mechanism that increases susceptibility to developing age-related pathologies, including cancer. In addition, NRF2/KEAP1 signaling is involved in chemoresistance and radioresistance occurrence in several types of cancers significantly worsening the outcome of the disease.

Thus, it is necessary to develop new therapeutic approaches that can improve diagnosis and treatment outcomes. Therefore, we need a better understanding of the molecular changes occurring in cancer pathogenesis to develop new molecular biomarkers able to predict tumor behavior and the risk of disease recurrence and chemoresistance. Moreover, understanding the molecular mechanisms involved in NRF2/KEAP1 modulation can significantly improve the therapeutic strategies used in cancer treatment.

This Special Issue, therefore, welcomes original research articles and reviews related to the role of NRF2/KEAP1 signaling in cancer. Communications, mini-reviews, systematic reviews and meta-analyses are also welcome.

We look forward to receiving your contributions.

Dr. Sonia Fantone
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • oxidative stress
  • cancer
  • aging
  • senescence
  • inflammation
  • ovarian cancer
  • prostate cancer
  • antioxidants

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Published Papers (2 papers)

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27 pages, 3321 KiB  
Article
Interplay of Cellular Nrf2/NF-κB Signalling after Plasma Stimulation of Malignant vs. Non-Malignant Dermal Cells
by Kristina Manzhula, Alexander Rebl, Kai Budde-Sagert and Henrike Rebl
Int. J. Mol. Sci. 2024, 25(20), 10967; https://doi.org/10.3390/ijms252010967 - 11 Oct 2024
Viewed by 2730
Abstract
Skin cancer is one of the most common malignancies worldwide. Cold atmospheric pressure Plasma (CAP) is increasingly successful in skin cancer therapy, but further research is needed to understand its selective effects on cancer cells at the molecular level. In this study, A431 [...] Read more.
Skin cancer is one of the most common malignancies worldwide. Cold atmospheric pressure Plasma (CAP) is increasingly successful in skin cancer therapy, but further research is needed to understand its selective effects on cancer cells at the molecular level. In this study, A431 (squamous cell carcinoma) and HaCaT (non-malignant) cells cultured under identical conditions revealed similar ROS levels but significantly higher antioxidant levels in unstimulated A431 cells, indicating a higher metabolic turnover typical of tumour cells. HaCaT cells, in contrast, showed increased antioxidant levels upon CAP stimulation, reflecting a robust redox adaptation. Specifically, proteins involved in antioxidant pathways, including NF-κB, IκBα, Nrf2, Keap1, IKK, and pIKK, were quantified, and their translocation level upon stimulation was evaluated. CAP treatment significantly elevated Nrf2 nuclear translocation in non-malignant HaCaT cells, indicating a strong protection against oxidative stress, while selectively inducing NF-κB activation in A431 cells, potentially leading to apoptosis. The expression of pro-inflammatory genes like IL-1B, IL-6, and CXCL8 was downregulated in A431 cells upon CAP treatment. Notably, CAP enhanced the expression of antioxidant response genes HMOX1 and GPX1 in non-malignant cells. The differential response between HaCaT and A431 cells underscores the varied antioxidative capacities, contributing to their distinct molecular responses to CAP-induced oxidative stress. Full article
(This article belongs to the Special Issue NRF2/KEAP1 Signalling in Cancer)
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Review

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22 pages, 1445 KiB  
Review
Nrf2 Signaling in Renal Cell Carcinoma: A Potential Candidate for the Development of Novel Therapeutic Strategies
by Valentina Schiavoni, Monica Emanuelli, Giulio Milanese, Andrea Benedetto Galosi, Veronica Pompei, Eleonora Salvolini and Roberto Campagna
Int. J. Mol. Sci. 2024, 25(24), 13239; https://doi.org/10.3390/ijms252413239 - 10 Dec 2024
Cited by 4 | Viewed by 1209
Abstract
Renal cell carcinoma (RCC) is the most common type of kidney cancer arising from renal tubular epithelial cells and is characterized by a high aggressive behavior and invasiveness that lead to poor prognosis and high mortality rate. Diagnosis of RCC is generally incidental [...] Read more.
Renal cell carcinoma (RCC) is the most common type of kidney cancer arising from renal tubular epithelial cells and is characterized by a high aggressive behavior and invasiveness that lead to poor prognosis and high mortality rate. Diagnosis of RCC is generally incidental and occurs when the stage is advanced and the disease is already metastatic. The management of RCC is further complicated by an intrinsic resistance of this malignancy to chemotherapy and radiotherapy, which aggravates the prognosis. For these reasons, there is intense research focused on identifying novel biomarkers which may be useful for a better prognostic assessment, as well as molecular markers which could be utilized for targeted therapy. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcriptional factor that has been identified as a key modulator of oxidative stress response, and its overexpression is considered a negative prognostic feature in several types of cancers including RCC, since it is involved in various key cancer-promoting functions such as proliferation, anabolic metabolism and resistance to chemotherapy. Given the key role of Nrf2 in promoting tumor progression, this enzyme could be a promising biomarker for a more accurate prediction of RCC course and it can also represent a valuable therapeutic target. In this review, we provide a comprehensive literature analysis of studies that have explored the role of Nrf2 in RCC, underlining the possible implications for targeted therapy. Full article
(This article belongs to the Special Issue NRF2/KEAP1 Signalling in Cancer)
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