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Cell Adhesion in Human Cancer
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Cell Adhesion in Human Cancer

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

Deadline for manuscript submissions: closed (1 May 2026) | Viewed by 7361

Special Issue Editors

Prof. Dr. Takashi Kojima

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Guest Editor
Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan
Interests: tight junctions; p63; pathophysiology; cell biology; molecular pathology; oncology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Makoto Osanai

E-Mail Website
Guest Editor
Department of Pathology, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan
Interests: vitamin D; tight junctions; pathophysiology; molecular pathology; oncology
Prof. Dr. Akira Ikari

E-Mail Website
Guest Editor
Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan
Interests: lung cancer; claudin; biological homeostasis; anticancer drug resistance; functional natural compounds; intercellular barrier

Special Issue Information

Dear Colleagues,

Cell-to-cell adhesion is a key element in epithelial tissue integrity and homeostasis. The loss of cell adhesion promotes epithelial to mesenchymal transition (EMT). Cadherin–catenin complexes are integral components of the adherens junctions crucial for cell–cell adhesion. The dysregulation of these complexes is linked to cancer development. Furthermore, tight junctions (TJs) are cell adhesion complexes that exist on the most apical side of the intercellular space between epithelial cells. TJs are composed of membrane proteins such as claudin (CLDN), occludin, and junctional adhesion molecules (JAMs), the tricellular TJ proteins angulin-1/lipolysis-stimulated lipoprotein receptor (LSR) and tricellulin, and scaffold proteins such as zonula occludens. The scaffold proteins including cingulin (CGN) connect with microtubules and actin. TJ proteins play roles beyond permeability barrier functions and control cell proliferation and differentiation. The abnormality of TJ proteins closely contributes to EMT and the malignancy of various cancers. The relation between TJs and the signal transduction pathways affects cancer cell growth, invasion, migration, and metabolism. This Special Issue on “Cell Adhesion in Human Cancer” will comprise a selection of original research papers and reviews focusing on the molecular mechanisms and the pathophysiology of cancer for the development of novel therapeutic and diagnostic approaches.

Prof. Dr. Takashi Kojima
Prof. Dr. Makoto Osanai
Prof. Dr. Akira Ikari
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

  • cell-to-cell adhesion
  • tight junctions
  • cytoskeleton
  • cancer
  • signal transduction pathways
  • transcriptional factors
  • EMT
  • cell metabolism
  • mechanical tension
  • human cells

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Published Papers (3 papers)

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Research

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23 pages, 11692 KB  
Article
The Role of Claudin-1 in Enhancing Pancreatic Cancer Aggressiveness and Drug Resistance via Metabolic Pathway Modulation
by Daisuke Kyuno, Hinae Asano, Reona Okumura, Kumi Takasawa, Akira Takasawa, Takumi Konno, Yuna Nakamori, Kazufumi Magara, Yusuke Ono, Masafumi Imamura, Yasutoshi Kimura, Takashi Kojima and Makoto Osanai
Cancers 2025, 17(9), 1469; https://doi.org/10.3390/cancers17091469 - 27 Apr 2025
Cited by 6 | Viewed by 2962
Abstract
Background/Objectives: Pancreatic ductal adenocarcinoma is a lethal malignancy, necessitating an understanding of its molecular mechanisms for the development of new therapeutic strategies. The tight junction protein claudin-1, known to influence cellular functions in various cancers and is considered a therapeutic target, remains unclear [...] Read more.
Background/Objectives: Pancreatic ductal adenocarcinoma is a lethal malignancy, necessitating an understanding of its molecular mechanisms for the development of new therapeutic strategies. The tight junction protein claudin-1, known to influence cellular functions in various cancers and is considered a therapeutic target, remains unclear in pancreatic cancer. Methods: This study assessed claudin-1 expression in resected pancreatic cancer samples, public databases, and pancreatic cancer cell lines. Claudin-1 knockout with CRISPR/Cas9 on poorly differentiated pancreatic cancer cell lines and a proteome analysis were performed to investigate the intracellular mechanisms of claudin-1. Results: Claudin-1 was markedly overexpressed in pancreatic ductal adenocarcinoma and intraepithelial neoplasia compared to normal ducts, and high claudin-1 levels were an independent predictor of poor prognosis. Claudin-1 knockout diminished cell proliferation, migration, invasion, and chemoresistance in pancreatic ductal adenocarcinoma. Proteome analysis revealed the significant downregulation of aldo-keto reductase family proteins (AKR1C2, AKR1C3, and AKR1B1) in claudin-1 knockout cells, which are linked to metabolic pathways. Aldo-keto reductase knockdown reduced chemoresistance, proliferation, and invasion in these cell lines. Conclusions: These findings indicate that the abnormal expression of claudin-1 promotes tumor progression and drug resistance through its interaction with aldo-keto reductase proteins, highlighting claudin-1 and aldo-keto reductase family proteins as potential biomarkers and therapeutic targets for pancreatic cancer. Full article
(This article belongs to the Special Issue Cell Adhesion in Human Cancer)
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19 pages, 11312 KB  
Article
Cholesterol Dietary Intake and Tumor Cell Homeostasis Drive Early Epithelial Tumorigenesis: A Potential Modelization of Early Prostate Tumorigenesis
by Marine Vialat, Elissa Baabdaty, Amalia Trousson, Ayhan Kocer, Jean-Marc A. Lobaccaro, Silvère Baron, Laurent Morel and Cyrille de Joussineau
Cancers 2024, 16(11), 2153; https://doi.org/10.3390/cancers16112153 - 6 Jun 2024
Cited by 3 | Viewed by 2527
Abstract
Epidemiological studies point to cholesterol as a possible key factor for both prostate cancer incidence and progression. It could represent a targetable metabolite as the most aggressive tumors also appear to be sensitive to therapies designed to decrease hypercholesterolemia, such as statins. However, [...] Read more.
Epidemiological studies point to cholesterol as a possible key factor for both prostate cancer incidence and progression. It could represent a targetable metabolite as the most aggressive tumors also appear to be sensitive to therapies designed to decrease hypercholesterolemia, such as statins. However, it remains unknown whether and how cholesterol, through its dietary uptake and its metabolism, could be important for early tumorigenesis. Oncogene clonal induction in the Drosophila melanogaster accessory gland allows us to reproduce tumorigenesis from initiation to early progression, where tumor cells undergo basal extrusion to form extra-epithelial tumors. Here we show that these tumors accumulate lipids, and especially esterified cholesterol, as in human late carcinogenesis. Interestingly, a high-cholesterol diet has a limited effect on accessory gland tumorigenesis. On the contrary, cell-specific downregulation of cholesterol uptake, intracellular transport, or metabolic response impairs the formation of such tumors. Furthermore, in this context, a high-cholesterol diet suppresses this impairment. Interestingly, expression data from primary prostate cancer tissues indicate an early signature of redirection from cholesterol de novo synthesis to uptake. Taken together, these results reveal that during early tumorigenesis, tumor cells strongly increase their uptake and use of dietary cholesterol to specifically promote the step of basal extrusion. Hence, these results suggest the mechanism by which a reduction in dietary cholesterol could lower the risk and slow down the progression of prostate cancer. Full article
(This article belongs to the Special Issue Cell Adhesion in Human Cancer)
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Review

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14 pages, 827 KB  
Review
Tight Spaces, Big Discoveries: Decoding Human Adhesion Biology with Avian Chorioallantoic Membrane Xenograft Models
by Niamh McAuley, Izabela Cymer, Robyn Stanley, Sinead Toomey, Catriona M. Dowling, Albert Leung, Ann M. Hopkins and Cathy E. Richards
Cancers 2026, 18(3), 508; https://doi.org/10.3390/cancers18030508 - 3 Feb 2026
Viewed by 793
Abstract
Tight junction (TJ) proteins, such as Junctional Adhesion Molecule-A (JAM-A), claudins, and occludin, play increasingly recognized roles in cancer biology beyond their structural functions, influencing tumour proliferation, invasion, metastasis and therapy resistance. Understanding how these proteins modulate tumour progression in vivo requires models [...] Read more.
Tight junction (TJ) proteins, such as Junctional Adhesion Molecule-A (JAM-A), claudins, and occludin, play increasingly recognized roles in cancer biology beyond their structural functions, influencing tumour proliferation, invasion, metastasis and therapy resistance. Understanding how these proteins modulate tumour progression in vivo requires models that are both physiologically relevant and ethically viable. The chick chorioallantoic membrane (CAM) xenograft model has emerged as a powerful and cost-effective in vivo system that aligns with the 3Rs (replacement, reduction, and refinement), offering unique advantages such as vascular accessibility, rapid tumour growth kinetics and immunotolerance. This review explores how the CAM model can be leveraged to study the mechanistic role of TJ proteins in tumour–stroma interactions, angiogenesis, extracellular matrix (ECM) remodelling and mechanotransduction, including the YAP/TAZ pathway. While limitations remain, particularly with respect to immune modelling and long-term studies, recent advances in imaging, genetic manipulation and integration of patient-derived xenografts (PDXs) are expanding the model’s translational relevance. Standardizing methodologies and embracing new molecular tools will further elevate the utility of this approach as a complementary platform to traditional rodent models, with significant promise for TJ-focused cancer research and therapeutic innovation. Full article
(This article belongs to the Special Issue Cell Adhesion in Human Cancer)
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