Tumor Biomechanics and Mechanobiology

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cancer Biology".

Deadline for manuscript submissions: 31 January 2027 | Viewed by 6029

Special Issue Editor


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Guest Editor
Key Laboratory for Biomechanics and Mechanobiology of Ministry of Education, Beijing Advanced Innovation Center for Biomedical Engineering, School of Biological Science and Medical Engineering, Beihang University, Beijing 100083, China
Interests: biomechanics; tumor cell microenvironment; macrophages; stem cell; genetics and genomics; molecular biology

Special Issue Information

Dear Colleagues,

Many studies have revealed the important role of mechanical forces in the progression of tumors. The interplay between mechanical and biochemical cues affects the function and behavior of tumor cells during the development of solid tumors, especially their metastatic potential. Based on the above information, clarifying mechanobiological transduction is beneficial in achieving a more systematic and comprehensive understanding of the complex regulatory network in the tumor microenvironment and is important in further research on how the mechanical microenvironment in the tumor affects the process of tumor occurrence and development.

We are pleased to invite you to submit relevant papers to our Special Issue, “Tumor Biomechanics and Mechanobiology”. We encourage submissions that investigate the migration, invasion, metastasis, and apoptosis of tumor cells and explore their mechanobiological role in tumor process, as well as their applications, such as in small molecules or gene-targeting entities in treating cancer.

This Special Issue will provide a platform for researchers to share their findings and contribute to the growing body of knowledge in pioneering research on the roles and mechanisms of biomechanics in tumor progression and innovative applications of cancer therapeutics in disease management.

For this Special Issue, submissions of original research articles and reviews are welcome. Research fields of interest include, but are not limited to, cancer biology, cell biology, genetics and genomics, and molecular biology.

I look forward to receiving your contributions.

Dr. Xinbin Zhao
Guest Editor

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Keywords

  • tumor migration
  • cancer cell invasion
  • cancer metastasis
  • biomechanics
  • tumor microenvironment
  • extracellular matrix
  • matrix degradation

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Published Papers (3 papers)

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Research

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22 pages, 6628 KB  
Article
The Chamber Gap Assay Is a Simple and Sensitive In Vitro Method for Studying Pancreatic Cancer-Induced Macrophage Recruitment and Morphological Alteration
by Maik Lenz, Stefanie Muliawan, Florian Nowak, Lea Miebach, Stephan Kersting, Tobias Schulze, Sander Bekeschus, Theresa Kordaß and Aydar Khabipov
Biology 2026, 15(3), 240; https://doi.org/10.3390/biology15030240 - 28 Jan 2026
Viewed by 780
Abstract
Pancreatic cancer is characterized by an immunosuppressive tumor environment in which macrophages are recruited and reprogrammed to support tumor growth. Studying macrophage migration and polarization is crucial for understanding disease progression and identifying therapeutic targets. However, existing in vitro methods such as the [...] Read more.
Pancreatic cancer is characterized by an immunosuppressive tumor environment in which macrophages are recruited and reprogrammed to support tumor growth. Studying macrophage migration and polarization is crucial for understanding disease progression and identifying therapeutic targets. However, existing in vitro methods such as the transwell assay provide limited spatial resolution and do not allow visualization of cell movement or morphological changes. Here, we established and evaluated the Chamber Gap Assay, a modified two-compartment culture system that enables direct, time-resolved observation and quantification of macrophage migration toward pancreatic cancer cells as well as phenotypic alterations. Using murine and human macrophage–cancer cell models, we compared the performance of the Chamber Gap Assay with the transwell assay. We found that macrophage monocultures displayed substantial spontaneous migration in the transwell system, while cancer cells induced only modest additional macrophage recruitment. In contrast, the Chamber Gap Assay demonstrated clear and highly significant directional macrophage movement toward cancer cells, with distinct migration patterns and improved sensitivity for detecting group differences. The method also enabled visualization of cancer cell movement within the same system. Furthermore, CGA offers observations of morphological changes in immune cells under the influence of pancreatic cancer cells. Our findings indicate that the Chamber Gap Assay provides a robust and physiologically relevant method for studying tumor-induced immune cell recruitment and associated morphological changes. Full article
(This article belongs to the Special Issue Tumor Biomechanics and Mechanobiology)
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Review

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34 pages, 1707 KB  
Review
Mimicking Gastric Cancer Collagen Reorganization with Decellularized ECM-Based Scaffolds
by Néstor Corro, Sebastián Alarcón, Ángel Astroza, Roxana González-Stegmaier and Carolina Añazco
Biology 2025, 14(8), 1067; https://doi.org/10.3390/biology14081067 - 16 Aug 2025
Cited by 3 | Viewed by 3644
Abstract
The tumor microenvironment (TME) has a substantial impact on the progression of gastric cancer. Collagen, the most abundant protein in the extracellular matrix (ECM), forms a dense physical barrier that regulates anti-tumor immunity in the TME. It is a significant regulator of the [...] Read more.
The tumor microenvironment (TME) has a substantial impact on the progression of gastric cancer. Collagen, the most abundant protein in the extracellular matrix (ECM), forms a dense physical barrier that regulates anti-tumor immunity in the TME. It is a significant regulator of the signaling pathways of cancer cells, which are responsible for migration, proliferation, and metabolism. ECM proteins, particularly remodeling enzymes and collagens, can be modified to increase stiffness and alter the mechanical properties of the stroma. This, in turn, increases the invasive potential of tumor cells and resistance to immunotherapy. Given the dynamic nature of collagen, novel therapeutic strategies have emerged that target both collagen biosynthesis and degradation, processes that are essential for addressing ECM stiffening. This review delineates the upregulation of the expression and deposition of collagen, as well as the biological functions, assembly, and reorganization that contribute to the dissemination of this aggressive malignancy. Furthermore, the review emphasizes the importance of creating 3D in vitro models that incorporate innovative biomaterials that avoid the difficulties of traditional 2D culture in accurately simulating real-world conditions that effectively replicate the distinctive collagen microenvironment. Ultimately, it investigates the use of decellularized ECM-derived biomaterials as tumor models that are designed to precisely replicate the mechanisms associated with the progression of stomach cancer. Full article
(This article belongs to the Special Issue Tumor Biomechanics and Mechanobiology)
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Other

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14 pages, 3620 KB  
Opinion
Sulforaphane as a Multi-Scale Mechano-Modulator in Cancer: An Integrative Perspective
by Xin Zhang, Lili Cheng, Yifan Han, Tailin Chen and Xinbin Zhao
Biology 2026, 15(2), 167; https://doi.org/10.3390/biology15020167 - 17 Jan 2026
Cited by 1 | Viewed by 1003
Abstract
Cancer progression is driven not only by biochemical signals but also by abnormal physical forces within a stiffened tumor microenvironment. This review re-examines the anticancer compound sulforaphane (SFN) through the integrative lens of tumor biomechanics. We propose SFN functions as a “mechano-modulator,” whose [...] Read more.
Cancer progression is driven not only by biochemical signals but also by abnormal physical forces within a stiffened tumor microenvironment. This review re-examines the anticancer compound sulforaphane (SFN) through the integrative lens of tumor biomechanics. We propose SFN functions as a “mechano-modulator,” whose pleiotropic effects converge to disrupt pro-invasive mechanotransduction. SFN targets key force-sensitive pathways (e.g., YAP/TEAD, Rho/ROCK), destabilizes invasion machinery (cytoskeleton, invadopodia), and promotes tissue-level changes such as extracellular matrix remodeling. While preclinical evidence for this mechano-modulatory role is compelling, this perspective also highlights the critical need for clinical validation and discusses the key translational challenges. By systematically linking SFN’s molecular actions to the biophysics of tumor progression, this synthesis provides a novel framework for understanding its efficacy and outlines a rational path for its future development as a mechano-inspired therapeutic. Full article
(This article belongs to the Special Issue Tumor Biomechanics and Mechanobiology)
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