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Pharmaceuticals
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Inhibition and Treatment in Adhesion, Migration, Invasion, and Metastasis of...
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Inhibition and Treatment in Adhesion, Migration, Invasion, and Metastasis of Cancer Cells

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: 25 December 2025 | Viewed by 6420

Special Issue Editors

Prof. Dr. Magdalena Izdebska

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Guest Editor
Department of Histology and Embryology, Faculty of Medicine, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 85-092 Bydgoszcz, Poland
Interests: cell biology; cytoskeleton; cell death; cancer cell culture; cancer biology; anticancer therapy
Dr. Marta Hałas-Wiśniewska

E-Mail Website
Guest Editor
Department of Histology and Embryology, Faculty of Medicine, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 85-092 Bydgoszcz, Poland
Interests: migration; invasion; cytoskeleton; cancer biology
Dr. Wioletta Arendt

E-Mail Website
Guest Editor
Department of Histology and Embryology, Faculty of Medicine, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 85-092 Bydgoszcz, Poland
Interests: cytoskeleton; cancer biology; metastasis; molecular therapeutic targets

Special Issue Information

Dear Colleagues,

Adhesion, migration, invasion and metastasis are key processes in the progression of cancer, representing critical steps through which cancer cells spread from their primary site to distant organs, leading to the establishment of secondary tumors. These processes are regulated by a complex network of signaling pathways that involve various molecules, including integrins, matrix metalloproteinases (MMPs) and the components of the extracellular matrix (ECM). The interactions between cancer cells and the ECM not only facilitate the physical movement of cells, but also activate signaling pathways that promote the survival, proliferation and further spread of cancer cells.

The ability of cancer cells to adhere, migrate and invade is closely linked to their phenotypic plasticity connected to phenomena such as the epithelial–mesenchymal transition (EMT), which is a critical mechanism for acquiring invasive properties. Furthermore, the tumor microenvironment plays a pivotal role in supporting and enhancing these processes through the secretion of growth factors, cytokines and chemokines, thereby creating a favorable niche for cancer progression.

This Special Issue seeks to gather original research articles and comprehensive reviews that explore the molecular mechanisms of these critical cancer progression steps and the development of therapeutic strategies to target them. Contributions may include studies on the molecular mechanisms regulating adhesion, migration, invasion and metastasis; the role of the tumor microenvironment in facilitating cancer cell mobility; advances in identifying molecular targets and developing inhibitors; preclinical and clinical investigations of novel therapeutic agents.

We look forward to your valuable contribution.

Prof. Dr. Magdalena Izdebska
Dr. Marta Hałas-Wiśniewska
Dr. Wioletta Arendt
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. Pharmaceuticals is an international peer-reviewed open access monthly 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

  • migration
  • metastasis
  • invasion
  • tumor progression
  • cell adhesion
  • cancer
  • epithelial–mesenchymal transition
  • cancer therapy

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Published Papers (3 papers)

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Research

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17 pages, 4873 KiB  
Article
Downregulation of Ezrin Suppresses Migration Potential in Cervical Cancer Cells
by Marta Hałas-Wiśniewska, Wioletta Arendt, Alina Grzanka and Magdalena Izdebska
Pharmaceuticals 2025, 18(1), 3; https://doi.org/10.3390/ph18010003 - 24 Dec 2024
Cited by 1 | Viewed by 727
Abstract
Background: The literature reports that ezrin (EZR) is important as a linker between microfilaments and cellular environments. Moreover, it affects cancer cell migration, but the exact mechanism is not fully understood. In this study, we aimed to investigate the role of EZR in [...] Read more.
Background: The literature reports that ezrin (EZR) is important as a linker between microfilaments and cellular environments. Moreover, it affects cancer cell migration, but the exact mechanism is not fully understood. In this study, we aimed to investigate the role of EZR in the migration of two different types of cervical cancer cells—from primary lesion (SiHa) and lymph node metastases (HT-3). In addition, we showed for the first time that a reduced EZR protein level affects the cellular response to the routinely used treatment with cisplatin. Methods: The most important stage of the study consisted of conducting a series of tests enabling the assessment of the migration potential of cervical cancer cells without altered EZR expression and with silenced protein expression. Results: Reducing the EZR level resulted in a decrease in the invasive and migration potential of SiHa and HT-3 cells’ inhibition of colony formation, a decrease in adhesive properties, and a strong reorganization of F-actin with a dominance of cells with a mitotic catastrophe phenotype. A lower level of protein significantly reduces the motor skills of SiHa and HT-3 cervical cancer cells. Conclusions: This significantly affects the assessment of EZR as a potential factor that can limit the development of metastases in targeted cancer therapy of cervical cancer. Full article
(This article belongs to the Special Issue Inhibition and Treatment in Adhesion, Migration, Invasion, and Metastasis of Cancer Cells)
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23 pages, 8689 KiB  
Article
Tight Junctions and Cancer: Targeting Claudin-1 and Claudin-4 in Thyroid Pathologies
by Jędrzej Borowczak, Dariusz Łaszczych, Katarzyna Olejnik, Jakub Michalski, Anna Gutowska, Monika Kula, Anita Bator, Marta Sekielska-Domanowska, Roman Makarewicz, Andrzej Marszałek, Łukasz Szylberg and Magdalena Bodnar
Pharmaceuticals 2024, 17(10), 1304; https://doi.org/10.3390/ph17101304 - 30 Sep 2024
Cited by 1 | Viewed by 2269
Abstract
Purpose: Claudins are tight junction proteins partaking in epithelial-mesenchymal transition and cancer progression. In this study, we investigated the expression patterns of claudin-1 and claudin-4 in thyroid pathologies, discussed their links with the pathogenesis of thyroid cancers, and reviewed the therapeutic potential of [...] Read more.
Purpose: Claudins are tight junction proteins partaking in epithelial-mesenchymal transition and cancer progression. In this study, we investigated the expression patterns of claudin-1 and claudin-4 in thyroid pathologies, discussed their links with the pathogenesis of thyroid cancers, and reviewed the therapeutic potential of targeting claudins in cancers. Methods: The research group 162 cores of thyroid samples from patients (70 female and 11 male) diagnosed with thyroid adenoma, goiter, papillary, medullary, and anaplastic thyroid cancers. All samples were stained for the expression of claudin-1 and claudin-4, and the analysis of IHC was performed. Results: Goiter samples showed negative claudin-1 and mostly positive expression of claudin-4. Papillary thyroid cancer and thyroid adenoma showed positive expression of claudin-1, while claudin-4 was positive in papillary thyroid cancers, goiters, and adenomas. In The Cancer Genome Atlas cohort, claudin-1 and claudin-4 were overexpressed in papillary thyroid cancer compared to normal thyroid tissues. Patients with high claudin-1 expression had significantly lower 5-year overall survival than patients with low claudin-1 levels (86.75% vs. 98.65, respectively). In multivariate analysis, high claudin-1 expression (HR 7.91, CI 95% 1.79–35, p = 0.006) and advanced clinical stage remained statistically significant prognostic factors of poor prognosis in papillary thyroid cancer. Conclusions: The pattern of claudin-1 staining was pathology-specific and changed between cancers of different histology. This phenomenon may be associated with the different pathogenesis of thyroid cancers and early metastasis. The loss of claudin-1 and claudin-4 characterized more aggressive cancers. Several studies have shown the benefits of targeting claudins in cancers, but their implementation into clinical practice requires further trials. Full article
(This article belongs to the Special Issue Inhibition and Treatment in Adhesion, Migration, Invasion, and Metastasis of Cancer Cells)
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Review

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18 pages, 2268 KiB  
Review
Cancer Metastases to the Liver: Mechanisms of Tumor Cell Colonization
by Wiktoria Andryszkiewicz, Piotr Misiąg, Anna Karwowska, Zofia Resler, Aleksandra Wojno, Julita Kulbacka, Anna Szewczyk and Nina Rembiałkowska
Pharmaceuticals 2024, 17(9), 1251; https://doi.org/10.3390/ph17091251 - 23 Sep 2024
Cited by 3 | Viewed by 2680
Abstract
The liver is one of the most common sites for metastasis, which involves the spread from primary tumors to surrounding organs and tissues in the human body. There are a few steps in cancer expansion: invasion, inflammatory processes allowing the hepatic niche to [...] Read more.
The liver is one of the most common sites for metastasis, which involves the spread from primary tumors to surrounding organs and tissues in the human body. There are a few steps in cancer expansion: invasion, inflammatory processes allowing the hepatic niche to be created, adhesions to ECM, neovascularization, and secretion of enzymes. The spread of tumor cells depends on the microenvironment created by the contribution of many biomolecules, including proteolytic enzymes, cytokines, growth factors, and cell adhesion molecules that enable tumor cells to interact with the microenvironment. Moreover, the microenvironment plays a significant role in tumor growth and expansion. The secreted enzymes help cancer cells facilitate newly formed hepatic niches and promote migration and invasion. Our study discusses pharmacological methods used to prevent liver metastasis by targeting the tumor microenvironment and cancer cell colonization in the liver. We examine randomized studies focusing on median survival duration and median overall survival in patients administered placebo compared with those treated with bevacizumab, ramucirumab, regorafenib, and ziv-aflibercept in addition to current chemotherapy. We also include research on mice and their responses to these medications, which may suppress metastasis progression. Finally, we discuss the significance of non-pharmacological methods, including surgical procedures, radiotherapy, cryotherapy, radiofrequency ablation (RFA), and transarterial embolization (TAE). In conclusion, the given methods can successfully prevent metastases to the liver and prolong the median survival duration and median overall survival in patients suffering from cancer. Full article
(This article belongs to the Special Issue Inhibition and Treatment in Adhesion, Migration, Invasion, and Metastasis of Cancer Cells)
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