Advances in Annexin Biology

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 28 October 2026 | Viewed by 933

Special Issue Editors


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Guest Editor
Department of Pharmacy, University of Salerno, Via Giovanni Paolo II 132, 84084 Fisciano, SA, Italy
Interests: skin wound healing; angiogenesis; endothelial to mesenchymal and epithelial to mesenchymal transition; cancer biology; cell transfection; in vitro cultures; wound healing in mice; cell migration and invasion; pharmacology in general; extracellular vesicles isolation, characterization and use
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Pharmacy, University of Salerno, Via Giovanni Paolo II 132, 84084 Fisciano, SA, Italy
Interests: annexin; cancer therapy; cancer biology; metastasis; cellular signaling; endothelial and epithelial-to-mesenchymal transition; extracellular vesicles; tumor microenvironment; biomarkers; skin wound healing
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Pharmacy, University of Salerno, Via Giovanni Paolo II 132, 84084 Fisciano, SA, Italy
Interests: anti-inflammatory activity; extracellular vesicles; cancer biology; cancer progression; epithelial to mesenchymal transition; cell migration and invasion; tumor microenvironment; in vitro tumor 3D models; tumor biomarkers; cellular behavior in response to pharmacological therapy

Special Issue Information

Dear Colleagues,

Annexins are a fascinating family of proteins that play crucial roles in how cells communicate, adapt, and respond to their environment. By binding to cell membranes in a calcium-dependent manner, annexins are involved in a wide range of cellular processes, including inflammation, membrane repair, signal transduction, apoptosis, and even from cancer development, differentiation to progression. In recent years, interest in annexins has grown significantly thanks to their biological relevance and to advances in high-resolution imaging techniques and the breakthroughs in molecular biology and gene editing tools. Together, these advances have transformed annexins from relatively obscure membrane-associated proteins into dynamic regulators of essential cellular processes. This growing understanding pays the way to new opportunities in the investigation of annexins as potential biomarkers and therapeutic targets in diseases where their expression could be dysregulated and functions notably affected. In this context, an example of one of the most intriguing aspects of annexin biology is their emerging role in tumor progression and in mediating the crosstalk between cancer cells and their surrounding microenvironment, a dynamic network of immune cells, stromal cells, extracellular matrix, and soluble factors. Additionally, annexins are known to further regulate the secretion of inflammatory mediators, extracellular vesicles (like exosomes), and even immune mechanisms both in physiological and pathological systems. By influencing these communication routes, annexins help create a microenvironment that supports tumor growth, angiogenesis, and immune suppression.

This Special Issue, "Advances in Annexin Biology," invites contributions that explore the multifaceted functions of annexins in cell behavior. We welcome original studies, reviews, and communications focused on how annexins act in both normal physiology and disease states. Whether you are studying their molecular mechanisms, interactions with other proteins or lipids, or their potential as therapeutic targets or biomarkers, this Special Issue aims to bring together a broad spectrum of insights.

Dr. Raffaella Belvedere
Prof. Dr. Antonello Petrella
Dr. Nunzia Novizio
Guest Editors

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Keywords

  • annexin family
  • calcium-dependent membrane binding
  • cell signaling
  • inflammation and immune response
  • membrane repair
  • cancer biology
  • cell motility
  • cell differentiation
  • tumor microenvironment
  • diagnostic/prognostic biomarkers
  • therapeutic targets

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Published Papers (1 paper)

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Research

15 pages, 3382 KB  
Article
A Thiadiazolopyrimidinone-Based Molecule Targeting Annexin A6 Impairs Cell Motility and Epithelial-to-Mesenchymal Transition in Pancreatic Cancer Cells Lacking Annexin A1
by Raffaella Belvedere, Nunzia Novizio, Dafne Ruggiero, Mariangela Palazzo, Ines Bruno, Stefania Terracciano and Antonello Petrella
Cells 2026, 15(4), 386; https://doi.org/10.3390/cells15040386 - 23 Feb 2026
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Abstract
Pancreatic carcinoma (PC) is the most lethal malignancy due to its aggressive behavior and limited therapeutic response. Among the annexin family, Annexin A1 (ANXA1) is documented to promote PC aggressiveness, and conversely, the role of Annexin A6 (ANXA6) is less explored. Here, we [...] Read more.
Pancreatic carcinoma (PC) is the most lethal malignancy due to its aggressive behavior and limited therapeutic response. Among the annexin family, Annexin A1 (ANXA1) is documented to promote PC aggressiveness, and conversely, the role of Annexin A6 (ANXA6) is less explored. Here, we report that ANXA6 is significantly upregulated in ANXA1 knockout (KO) MIA PaCa-2 cells. Using LAM20, our previously identified ANXA6 modulator, we show that inhibition of this protein impairs cell motility, and epithelial-to-mesenchymal transition markers, without affecting 2D/3D cell proliferation. ANXA6 siRNA-mediated knockdown reproduces LAM20 effects, suggesting a relationship with their impact on ANXA6. Interestingly, in ANXA1 KO cells, LAM20 reduced the migration/invasion rate differently from the ANXA1 inhibitor heparan sulfate, which retains effects on the wild-type (WT) MIA PaCa-2 counterpart. These findings suggest that in cells lacking ANXA1, ANXA6 plays a compensatory role in sustaining the aggressive phenotype, albeit to a lesser extent than in WT cells. Thus, LAM20 represents a promising therapeutic strategy to impair PC aggressiveness. Our study provides new insights into ANXA1/ANXA6 crosstalk and introduces a novel approach to disturb PC pro-invasive mechanisms. Targeting ANXA1 and ANXA6 is relevant because, where ANXA1 is downregulated/absent, ANXA6 expression can be restored in a compensatory manner, partially sustaining tumor progression. Full article
(This article belongs to the Special Issue Advances in Annexin Biology)
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