The heartbeat helps slow the growth of tumors in cardiac tissue. This is the finding of an international study published in Science, coordinated by the University of Trieste in collaboration with the International Centre for Genetic Engineering and Biotechnology (ICGEB) and the Monzino Cardiology Center IRCCS. 

The study, entitled Mechanical load inhibits tumor growth in mouse and human hearts, draws attention to a still little-explored aspect of cancer biology: the physical forces acting in the myocardium do not merely regulate heart function, but can also influence the behavior of tumor cells, even to the point of slowing their proliferation. 

The research involved partners in Italy, Austria, Germany, Norway, and the United Kingdom, including the European Institute of Oncology, the Medical University of Innsbruck, King’s College London, the University Medical Center Hamburg-Eppendorf, and the Simula Research Laboratory in Oslo. This broad and integrated network made it possible to combine experimental, clinical, bioengineering, and computational expertise. 

The work began from a medical observation that has long been known but remains only partly understood in its underlying mechanisms: the heart develops tumors very rarely and, even when it is affected by metastases, these tend to be smaller than those found in other organs. The researchers therefore investigated whether one explanation might lie precisely in the mechanical nature of cardiac tissue, which is constantly subjected to contraction, pressure, and deformation. 

To do so, they used different and innovative experimental models. On the one hand, they studied what happens when the heart is mechanically “unloaded”: under these conditions, tumor cells proliferate much more extensively. On the other hand, they used engineered cardiac tissues grown in the laboratory, where they were able to modulate mechanical load and directly observe the response of tumor cells. 

The result was consistent: when cardiac tissue beats and generates mechanical load, tumor growth slows down; when this stimulus is reduced, tumor cells resume proliferating. 

“Our findings show that cardiac pulsation is not only a physiological function, but can also act as a natural suppressor of tumor growth,” said Professor Serena Zacchigna, Professor of Molecular Biology at the University of Trieste and head of the Cardiovascular Biology laboratory at ICGEB. “This suggests that the cardiac environment is unfavorable to tumor cells not only for immunological or metabolic reasons, but also because its continuous mechanical activity physically limits their expansion.” 

Professor Giulio Pompilio, Scientific Director of the Monzino Cardiology Center IRCCS and Professor of Cardiac Surgery at the Department of Biomedical, Surgical and Dental Sciences of the University of Milan, added: “One of the most fascinating aspects of this research is that it shows how the mechanical forces regulating heart activity, already known to create an environment hostile to its regenerative ability, conversely exert a beneficial biological action in counteracting tumor growth. Perhaps these are two sides of the same coin. I would also like to stress that this work was made possible thanks to the collaboration of experts from different fields, ranging from cardiology to oncology, bioengineering, and bioinformatics.” 

The most interesting finding concerns the level at which this effect occurs. The study shows that the mechanical forces exerted by the heart do not stop at the surface of tumor cells, but also affect internal mechanisms that regulate their ability to multiply. 

This is an important step because it concretely links the mechanical dimension of the cellular environment with the epigenetic regulation of the tumor. In other words, the heart may be hostile to tumor cells not only for immunological or metabolic reasons, but also because its very movement physically limits their expansion. 

Another major strength of the study lies in its ability to connect basic research with clinical observation. The results obtained in experimental models were compared with human cardiac metastases, analyzed in parallel with lesions located in other organs of the same patients. This made it possible to verify that the molecular signatures observed in the laboratory are also found in human samples, reinforcing the robustness of the work and its potential impact. 

This research opens up a potentially transformative direction: understanding whether and how mechanical stimuli might one day be harnessed as a therapeutic tool against cancer. The idea that a “mechanical therapy” could complement or inspire new oncological strategies still remains to be developed, but the principle emerging from the study is clear: physical forces are not just a backdrop to disease, but could represent an important brake on it.