The study

If the heart stops the tumour: how the heartbeat slows the proliferation of 'bad' cells

The physical forces generated by the heart muscle can hinder tumour growth in the tissue: in Science the study coordinated by the University of Trieste in collaboration with the International Centre for Genetic Engineering and Biotechnology and Irccs Monzino

by Health Review

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3' min read

Translated by AI
Versione italiana

3' min read

Translated by AI
Versione italiana

This work started from an observation known in medicine, but still little understood in terms of its mechanisms: the heart very rarely develops tumours and, even when metastases do occur, they tend to be smaller than those in other organs. Hence the logical step: the researchers investigated whether one of the explanations might lie in the mechanical nature of heart tissue, which is constantly subjected to contraction, pressure and deformation. The conclusion - entrusted to an international study published in Science, co-ordinated by the University of Trieste in collaboration with the International Centre for Genetic Engineering and Biotechnology (ICGEB) and the Centro Cardiologico Monzino Irccs - is that the beating of the heart helps to slow down the growth of tumours in heart tissue.

The Studio

The work, entitled 'Mechanical load inhibits tumour growth in mouse and human hearts', draws attention to a hitherto little-studied aspect: the physical forces acting in the myocardium do not only regulate cardiac function, but can also influence the behaviour of tumour cells, to the point of slowing down their proliferation.

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The study involves partners in Italia, Austria, Germany, Norway and the UK, including the European Institute of Oncology, Medical University of Innsbruck, King's College London, University Medical Center Hamburg-Eppendorf, Simula Research Laboratory in Oslo. A broad and integrated network has allowed the combination of experimental, clinical, bioengineering and computational expertise.

The models

In their study, the researchers used different and innovative experimental models. On the one hand, they studied what happens when the heart is mechanically 'unloaded': under these conditions, cancer cells proliferate much more. On the other, they used lab-engineered heart tissue, in which it was possible to modulate the mechanical load and directly observe the response of the tumour cells. The result was consistent: when the heart tissue beats and generates mechanical load, tumour growth slows down; when this stimulus is reduced, the tumour cells start proliferating again.

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

'One of the most fascinating aspects of this research is that it has revealed that the mechanical forces that regulate the activity of the heart, known to determine an environment hostile to its regenerative ability, conversely exert a beneficial biological action in counteracting tumour growth,' adds Giulio Pompilio, Scientific Director of the Centro Cardiologico Monzino Irccs: 'Perhaps these are two sides of the same coin. I also feel it is important to emphasise that this work has been possible thanks to the collaboration of experts in different fields, from cardiology to oncology, bioengineering and bioinformatics'.

Tumour cell "tablets"

The most interesting finding concerns the level at which this effect manifests itself. Indeed, the work shows that the mechanical forces exerted by the heart do not stop at the surface of tumour cells, but also affect certain 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 tumour. In other words, the heart would not only be hostile to tumour cells for immunological or metabolic reasons, but also because its very movement physically limits their expansion.

The "mechanical therapy"

Another element of great value is the study's ability to link basic research and clinical observation. The results obtained in the experimental models were in fact compared with human cardiac metastases, analysed 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, strengthening the soundness of the work and its potential impact.

The research opens up a transformative direction: understanding whether and how mechanical stimuli could be exploited as a therapeutic lever against cancer in the future. The idea that 'mechanical therapy' could flank or inspire new cancer strategies has yet to be developed, but the principle that emerges from the study is clear: physical forces are not merely a context of the disease, but could be an important brake on it.

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