Despite the heart being well vascularized, primary cardiac tumours and metastases are rare. However, the underlying mechanisms that limit tumour establishment and growth remained incompletely understood. In a recent study, Ciucci, Lorizio et al. show that mechanical load reduces cancer cell proliferation in the myocardium.

In an ex vivo engineered heart tissue (EHT) system, composed of neonatal rat cardiomyocytes and fibroblasts and engineered to regulate mechanical load at will, tumour growth mirrored the in vivo situation: unloading promoted proliferation whereas overloading suppressed it. To model prolonged unloading in vitro, a modified EHT system was used in which cardiomyocyte contractility was controlled by calcium, generating static (no calcium) and beating (with calcium) EHTs. Cancer cells proliferated more in static EHTs whereas proliferation rate was markedly reduced in beating tissues. Furthermore, in beating EHTs, cancer cells localized to the outer layers, where hydrostatic pressure is lower.