Mechanical load as an endogenous tumor suppressor: Nesprin-2-mediated mechanotransduction reshapes the cancer epigenome

Mechanical load as an endogenous tumor suppressor: Nesprin-2-mediated mechanotransduction reshapes the cancer epigenome. Download PDF Subjects Cancer genomics Cancer microenvironment In a recent study published in Science, Ciucci et al. Show that physiological mechanical loading suppresses cancer cell proliferation in the heart through Nesprin-2-dependent nuclear mechanotransduction and epigenetic remodeling.

1 These findings identify cardiac mechanics as an endogenous barrier to cancer and suggest new mechanically and epigenetically informed therapeutic strategies. Why does a highly vascularized organ that is continuously exposed to circulating tumor cells so rarely develop primary tumors or myocardial metastases. This paradox has usually been framed through the “seed-and-soil” concept, emphasizing the myocardium’s metabolic, cellular, and extracellular peculiarities.

Cancer mechanobiology, meanwhile, has largely focused on tumor-promoting matrix stiffness and mechanosensitive signaling. 2 Yet, force is not an unitary stimulus, because its biological consequences depend on its magnitude, direction, periodicity, and the surrounding tissue architecture, while compressive stress can also restrain proliferation. 3 The study’s strength lies in triangulation across several experimental models.

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