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Cancers
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Hypoxia-Targeting Strategies to Improve Cancer Therapy Outcomes
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Hypoxia-Targeting Strategies to Improve Cancer Therapy Outcomes

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 561

Special Issue Editors

Dr. Roben Gieling

E-Mail Website
Guest Editor
Faculty of Science and Environment, School of Geography and Natural Sciences, University of Northumbria, Newcastle Upon Tyne NE1 8ST, UK
Interests: hypoxia; hypoxia-inducible factor 1 signaling; tumor microenvironment; tumor-associated immunity; molecular targeted therapies; nanoparticle delivery
Special Issues, Collections and Topics in MDPI journals
Dr. Ayse Latif

E-Mail Website
Guest Editor
School of Health Sciences, Division of Pharmacy and Optometry, University of Manchester, Manchester M13 9PL, UK
Interests: hypoxia; MRI; perfusion imaging

Special Issue Information

Dear Colleagues,

Tumor hypoxia remains one of the most persistent and clinically significant barriers to effective cancer treatment. Low oxygen levels within tumors not only promote aggressive phenotypes but also drive resistance to chemotherapy, radiotherapy, targeted agents, and immunotherapies. For researchers, this presents both a critical challenge and a unique opportunity: targeting hypoxia to improve the outcomes of traditional and novel cancer therapies. In recent years, there has been growing momentum around the development of hypoxia-targeted strategies, including hypoxia-activated prodrugs, inhibitors of hypoxia-inducible factors (HIFs) and their target genes, oxygen-modifying agents, and precision drug delivery systems. These approaches are increasingly being integrated into combination therapy regimens, with promising results in preclinical and clinical settings. This Special Issue, titled "Hypoxia-Targeting Strategies to Improve Cancer Therapy Outcomes," gathers original research and review papers that highlight the recent advances at the intersection of tumor biology, drug development, translational research, and clinical practice that underscore how understanding and intervening in hypoxic signaling can sensitize tumors to traditional and novel treatments and overcome entrenched resistance mechanisms.

Dr. Roben Gieling
Dr. Ayse Latif
Guest Editors

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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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. Cancers is an international peer-reviewed open access semimonthly 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

  • tumor hypoxia
  • cancer therapy resistance
  • hypoxia-targeted therapy
  • hypoxia-inducible factors (HIFs)
  • hypoxia-activated prodrugs
  • oxygen-modifying agents
  • combination therapy
  • precision drug delivery
  • tumor microenvironment
  • translational cancer research

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Published Papers (1 paper)

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Research

24 pages, 5708 KB  
Article
Hypoxia-Inducible Factor-1α, a Novel Molecular Target for a 2-Aminopyrrole Derivative: Biological and Molecular Modeling Study
by Svetlana S. Zykova, Tatyana Gessel, Aigul Galembikova, Evgenii S. Mozhaitsev, Sophia S. Borisevich, Nazim Igidov, Emiliya S. Egorova, Ekaterina Mikheeva, Natalia Khromova, Pavel Kopnin, Alina Galyautdinova, Vladimir Luzhanin, Maxim Shustov and Sergei Boichuk
Cancers 2026, 18(1), 115; https://doi.org/10.3390/cancers18010115 - 30 Dec 2025
Viewed by 348
Abstract
Background: Hypoxia-inducible factor-1α (HIF-1α) is a well-known transcriptional regulator that mediates a broad spectrum of cellular responses to hypoxia, including angiogenesis, extracellular matrix remodeling, and metabolic reprogramming. These activities can be achieved by upregulation of numerous genes, such as vascular endothelial growth factors, [...] Read more.
Background: Hypoxia-inducible factor-1α (HIF-1α) is a well-known transcriptional regulator that mediates a broad spectrum of cellular responses to hypoxia, including angiogenesis, extracellular matrix remodeling, and metabolic reprogramming. These activities can be achieved by upregulation of numerous genes, such as vascular endothelial growth factors, fibroblast growth factors, and platelet-derived growth factors, which are involved in the growth regulation of normal tissues and solid tumors. Notably, HIF-1α-mediated regulation of the solid tumor’s microenvironment effectively modulates tumor sensitivity to anticancer therapies and thereby can contribute to disease progression. Methods: The study was performed on breast, lung and prostate cancer cell lines. Protein expression was examined by western blotting. Antitumor activity of 2-ANPC was measured by syngeneic 4T1 breast cancer mouse model. Results: We show here that a 2-aminopyrrole derivative (2-amino-1-benzamido-5-(2-(naphthalene-2-yl)-2-oxoethylidene)-4-oxo-4,5-dihydro-1-H-pyrrole-3-carboxamide—2-ANPC), previously shown as a potent microtubule-targeting agent, effectively downregulates HIF-1α expression in a broad spectrum of cancer cell lines, including breast, lung, and prostate cancer. The downregulation of HIF-1α expression in 2-ANPC-treated cancer cells was due to enhanced proteasome-mediated degradation, whereas the proteasome inhibitor MG-132 effectively reversed this downregulation. 2-ANPC’s potency in downregulating HIF-1α was also shown in vivo by using the 4T1 breast cancer syngraft model. Importantly, this 2-aminopyrrole derivative also downregulated the expression of vascular endothelial growth factor receptors 1 and 3 (VEGFR1 and 3) in 4T1 tumors, which correlated with decreased tumor weight and size. As expected, an increase in apoptotic (i.e., cleaved caspase-3-positive) cells was detected in 4T1 tumors treated with 2-aminopyrrole derivative. Lastly, using various computational tools, we identified four potential binding sites for 2-ANPC to interact with HIF-1α, HIF-1β, and the p300 complex. Conclusions: Collectively, we show here, for the first time, that HIF-1α is a novel molecular target for the 2-aminopyrrole derivative (2-ANPC), thereby illustrating it as a potential scaffold for the development of potent chemotherapeutic agents with anti-angiogenic activity. Full article
(This article belongs to the Special Issue Hypoxia-Targeting Strategies to Improve Cancer Therapy Outcomes)
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