Key result
Mechanical load reduces myocardial cancer cell proliferation by decreasing chromatin compaction and histone methylation via Nesprin-2.
Why the study?
Because the heart rarely develops cancer and lacks regenerative capacity, mechanisms limiting cardiac regeneration may also protect against cancer, prompting investigation into the role of mechanical load.
Does mechanical load reduce cancer cell proliferation in the myocardium?
Does mechanical load reduce cancer cell proliferation in the myocardium?
Mechanical forces protect the heart from cancer by reducing cancer cell proliferation via Nesprin-2 mediated chromatin changes, suggesting potential mechanical stimulation-based cancer therapies.
The heart rarely develops cancer, and, at the same time, it lacks regenerative capacity, as cardiomyocytes stop proliferating after birth. This suggests that mechanisms limiting cardiac regeneration may also protect against cancer. In this work, we investigated the role of mechanical load and used in vivo cancer models and ex vivo engineered heart tissues to show that mechanical load reduces cancer cell proliferation in the myocardium. Spatial transcriptomics of human cardiac metastases revealed decreased histone methylation and chromatin compaction. These changes affect chromatin accessibility at proliferation-related loci, with Nesprin-2 identified as a key mechanosensor. Our results uncover how mechanical forces protect the heart from cancer and suggest potential strategies for cancer therapy based on mechanical stimulation.
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Ciucci et al. (2026) studied Cardiac cancer and metastases. Mechanical load was evaluated on Cancer cell proliferation. Mechanical load reduces cancer cell proliferation in the myocardium by decreasing histone methylation and chromatin compaction via the mechanosensor Nesprin-2.
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