Addressing the Role of Mechanical Forces on Nucleus and Chromatin Dynamics in Cancer Development and Metastasis

Cancer biology is a dynamically evolving field that continually seeks to unravel the complexities of tumorigenesis and metastasis. Despite advancements in identifying molecular pathways and cellular processes, the precise mechanisms, especially those involving mechanical forces on the cell nucleus, remain partially understood. Emerging evidence suggests that mechanical stresses, particularly in the context of the tumor microenvironment, play a pivotal role in cancer progression. Increased tissue stiffness and the altered fibrous architecture around tumors exert significant influence over cellular structures, impacting chromatin organization and the overarching nuclear architecture in cancerous cells.

Recent studies have highlighted the critical importance of nuclear mechanics in understanding metastasis, with nuclear deformability recognized as a crucial factor. The transmission of mechanical stresses from the tumor microenvironment through the cytoskeleton affects chromatin configuration, altering the gene expression landscape. These disruptions often precipitate epigenetic changes, contributing to malignancy and altering the natural course of cellular behavior. By examining these biomechanical interactions, researchers are gaining insights into the potential mechanochemical switches and pathways activated during oncogenesis.

This Research Topic aims to explore the intersection of mechanical forces and cancer biology, focusing on nuclear mechanics as a conduit for understanding malignancy. By targeting mechanobiological insights, we wish to reveal novel "mechanotargets"—key regulators influenced by mechanical stress that contribute to tumorigenic processes. This approach opens new prospects for developing or repurposing therapeutic strategies designed to counteract these oncogenic modifications induced by mechanical stimuli.

To gather further insights into the mechanobiological influences on cancer and surrounding tissues, we welcome articles addressing, but not limited to, the following themes:

- Cell nucleus shape and composition and its variation in cancer and metastasis.
- Impact of chromatin remodelling and epigenetic modification in cancer development.
- Heterochromatin/euchromatin balance alteration in cancer.
- Chromatin/cell nucleus/cell cytoskeleton axis role in cancer and metastasis.
- Impact of the mechanical forces generated by cancer cells on normal cells’ nucleus shape and chromatin.


Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Case Report
• Clinical Trial
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Mini Review
• Original Research
• Perspective
• ... View all formats

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Case Report
• Clinical Trial
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Mini Review
• Original Research
• Perspective
• Review
• Systematic Review

Keywords: Mechanical forces, cell nucleus, chromatin dynamics, epigenetics, cancer, metastasis.

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.