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Cells
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Cellular Mechanisms of Anti-Cancer Therapies
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Cellular Mechanisms of Anti-Cancer Therapies

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 1794

Special Issue Editors

Dr. Ilgen Mender

E-Mail Website
Guest Editor
MAIA Biotechnology, Inc., Chicago, IL, USA
Interests: anti-cancer therapies; targeted therapies; immunotherapy; anti-tumor immunity; personalized medicine; telomeres; telomerase
Dr. Kazuyuki Kitatani

E-Mail Website
Guest Editor
Laboratory of Immunopharmacology, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata 573‐0101, Japan
Interests: sphingolipids; ceramides; sphingotherapy; cancer therapy; cancer biology; cancer metastasis; cellular signaling; cell death; necroptosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer cells possess distinct cellular mechanisms that enable them to replicate and function differently from normal cells. During the transition from normal to malignant phases, tumor cells acquire various characteristics and capabilities, which may be influenced by the localization of this transformation, leading to the emergence of multiple tumor types and subtypes, each with unique aberrations. Various approaches have been developed to target cancer cells, including targeted therapy, chemotherapy, radiation therapy, immunotherapy, and more. These anti-cancer therapies employ various mechanisms at the cellular level to disrupt cancer cells by inducing apoptosis, inhibiting cell proliferation, disrupting DNA repair, and interfering with signaling pathways. Understanding the cellular mechanisms of anti-cancer drugs provides advantages in developing therapies, enhancing efficacy, personalizing medicine, predicting drug resistance, and identifying biomarkers for improved cancer treatment strategies. Experimental biology and systems biology have improved our understanding of cellular mechanisms, but more research is needed to fully elucidate the complexities of these pathways, including the interplay between cancer cells and the immune system, develop innovative therapies, and address challenges such as drug resistance and response variability in cancer treatment. We welcome any articles that address cellular mechanisms of anti-cancer drugs in various contexts.

Dr. Ilgen Mender
Dr. Kazuyuki Kitatani
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 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. Cells 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 2700 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

  • anti-cancer therapies
  • innovative treatment strategies
  • cellular mechanisms
  • drug resistance
  • personalized medicine

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Published Papers (2 papers)

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Research

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25 pages, 3757 KiB  
Article
GATAD2B O-GlcNAcylation Regulates Breast Cancer Stem-like Potential and Drug Resistance
by Giang Le Minh, Jessica Merzy, Emily M. Esquea, Nusaiba N. Ahmed, Riley G. Young, Ryan J. Sharp, Tejsi T. Dhameliya, Bernice Agana, Mi-Hye Lee, Jennifer R. Bethard, Susana Comte-Walters, Lauren E. Ball and Mauricio J. Reginato
Cells 2025, 14(6), 398; https://doi.org/10.3390/cells14060398 - 8 Mar 2025
Viewed by 834
Abstract
The growth of breast tumors is driven and controlled by a subpopulation of cancer cells resembling adult stem cells, which are called cancer stem-like cells (CSCs). In breast cancer, the function and maintenance of CSCs are influenced by protein O-GlcNAcylation and the enzyme [...] Read more.
The growth of breast tumors is driven and controlled by a subpopulation of cancer cells resembling adult stem cells, which are called cancer stem-like cells (CSCs). In breast cancer, the function and maintenance of CSCs are influenced by protein O-GlcNAcylation and the enzyme responsible for this post-translational modification, O-GlcNAc transferase (OGT). However, the mechanism of CSCs regulation by OGT and O-GlcNAc cycling in breast cancer is still unclear. Analysis of the proteome and O-GlcNAcome, revealed GATAD2B, a component of the Nucleosome Remodeling and Deacetylase (NuRD) complex, as a substrate regulated by OGT. Reducing GATAD2B genetically impairs mammosphere formation, decreases expression of self-renewal factors and CSCs population. O-GlcNAcylation of GATAD2B at the C-terminus protects GATAD2B from ubiquitination and proteasomal degradation in breast cancer cells. We identify ITCH as a novel E3 ligase for GATAD2B and show that targeting ITCH genetically increases GATAD2B levels and increases CSCs phenotypes. Lastly, we show that overexpression of wild-type GATAD2B, but not the mutant lacking C-terminal O-GlcNAc sites, promotes mammosphere formation, expression of CSCs factors and drug resistance. Together, we identify a key role of GATAD2B and ITCH in regulating CSCs in breast cancer and GATAD2B O-GlcNAcylation as a mechanism regulating breast cancer stem-like populations and promoting chemoresistance. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Anti-Cancer Therapies)
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Review

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16 pages, 843 KiB  
Review
The Role of A20 in Cancer: Friend or Foe?
by Jinju Lee and Heesun Cheong
Cells 2025, 14(7), 544; https://doi.org/10.3390/cells14070544 - 4 Apr 2025
Viewed by 507
Abstract
A20 is a ubiquitin-editing enzyme that has emerged as a key regulator of inflammatory signaling with paradoxical roles in cancer. Acting as both an oncogene and a tumor suppressor gene depending on the cellular context, A20 modulates important cell pathways, such as NF-κB [...] Read more.
A20 is a ubiquitin-editing enzyme that has emerged as a key regulator of inflammatory signaling with paradoxical roles in cancer. Acting as both an oncogene and a tumor suppressor gene depending on the cellular context, A20 modulates important cell pathways, such as NF-κB signaling and autophagy. In this review, we summarize the dual roles of A20 in tumorigenesis, highlighting its ability to promote tumor progression in cancers, such as breast and melanoma, while functioning as a tumor suppressor in lymphomas and hepatocellular carcinoma. We discuss the interplay of A20 with autophagy, a process that is important for maintaining cellular homeostasis and influencing tumor dynamics. By integrating recent findings, we provide insight into how dysregulation of A20 and its associated pathways can either suppress or drive cancer development, which may lead to improved therapeutic intervention. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Anti-Cancer Therapies)
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