Mechanobiology and Tumor Microenvironment

Dear Colleagues,

Emerging evidence has revealed that mechanical cues generated by matrix environmental and cell stiffness can regulate transcriptional programs in cells and contribute to different cancer phenotypes. To adapt and survive in the tumor microenvironment, cancer cells actively respond to the mechanical perturbations from extracellular matrixes, blood vessels, stroma cells, and other tumor-infiltrating lymphocytes. Interestingly, alterations in cell–cell contact and cell–matrix adhesion have been found to modulate metabolic pathways in cells undergoing invasion and anchorage-independent growth. During these processes, cytoskeleton proteins play important roles in linking mechanical cues from cell adhesion molecules to cell nucleus via the linker of the nucleoskeleton and cytoskeleton (LINC) complex, leading to chromatin structural changes and gene expression alterations. In recent years, long-lived cytoskeletal structures have been proposed to act as epigenetic determinants of cell shape, function, and fate, which can even generate “memory” in cells to influence their future behavior.

On the other hand, studies on nuclear architecture have revealed that replication stress caused by lamin dysfunction has resulted in genome instability and DNA breaks/damages, leading to chronic inflammation by cGAS-STING activation. This finding provides a molecular link to convert mechanical stress into cancer cell evolution via long-term exposure and selection of DNA damage/sensing responses. Type I IFN is the downstream effector of the cGas-STING pathway, which subsequently triggers cell senescence, autophagy or cell death. Clinical studies have confirmed that chronic inflammation/long-term cGAS-STING activation caused by genome instability functions as a driving force to enrich cell clones with more aggressive phenotypes. Defects in the DNA sensing pathway are thus considered a mechanism in cancer to escape immune surveillance.

This Special Issue will discuss how disturbances in the mechanical properties of cells can modulate cancer aggressiveness and determine the tumor microenvironment via alterations in mechano-transduction. Original manuscripts and reviews dealing with any aspect of mechanobiology in cancer development and related pathophysiology are highly welcome.

Prof. Jim Jinn-Chyuan Sheu
Guest Editor

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• mechano-transduction
• microenvironment
• cancer evolution/cloncal selection
• cell stemness
• cytoskeleton
• cell adhesion/migration/invasion