The discovery of an alternative communication pathway within cells, a sort of ‘molecular Intranet’, could lead to new treatments for tumors. This is the prospect opened by a study signed by scientists from the European Institute of Oncology (IEO) and the University of Milan, funded by the Airc Foundation for Cancer Research and by the EU through the ERC (European Research Council). The results are published in ‘Nature Communications’.
On their surface – explain Ieo and UniMi – cells have receptors that act like antennas: they receive signals from the outside world, which they intercept and transfer inside the cell. These signals are vitally important, because they generate specific behavioral instructions. When a receptor binds to an external signal molecule, it triggers a cascade of chemical reactions inside the cell, which eventually reaches the nucleus, the control center. Here the instructions are received and processed in order to generate a specific cellular response. Depending on which one it is, the cell can act in different ways: for example, it can move in a certain direction or divide into two daughter cells. Until recently, it was believed that this long-range communication, from the cell surface to the nucleus, was the only way in which cells could respond to an external stimulus. The study instead reveals the existence of another pathway, a ‘plan B’ for intracellular communication, which tumors could override and which may therefore represent a new therapeutic target.
“Our research – explains Sara Sigismund, scientific director of the study, researcher at the Department of Molecular Oncology IEO and associate professor at Statale – has revealed that a particular receptor for growth factors, known as Egfr, can communicate directly with some organelles inside the cell. Egfr are involved in many essential biological functions such as proliferation, survival or migration, but also in diseases such as cancer. We have shown that, when these receptors are activated by high concentrations of a specific growth factor, some organelles inside the cell approach the cell surface where the activated receptors are located. Among these organelles are the endoplasmic reticulum, a system of intercommunicating membranes of the cell, and the mitochondria, responsible for energy production. Thanks to their movement, the activated receptors can interact directly with the endoplasmic reticulum and mitochondria, influencing their metabolic function and causing an increase in energy production, with a double result”.
“On the one hand – the scientist describes – the removal of the receptor from the cell surface and its degradation is promoted. The consequence is the elimination of the ‘antennas’ for growth factors which, no longer finding receptors to bind to, are no longer able to transmit their proliferation orders to the cell. On the other hand, the cellular machinery responsible for cell movement is stimulated. Therefore, the internal communication network between organelles seems to be important to ensure an adequate cellular response to high concentrations of growth factor: a reaction capable of inhibiting cell growth and promoting the movement of the cell itself. This network could be altered in tumors”.
“Cell proliferation and movement – comments Pier Paolo Di Fiore, head of the Novel Diagnostics Program at IEO, professor at UniMi and co-author of the article – are two key functions for the development of tumors in the body. The first is responsible for tumor growth, while movement can give rise to metastases. The identification of this communication pathway could therefore provide the basis for studies aimed at developing new anticancer therapies. In fact, it would be possible to interfere with this pathway by blocking unwanted cellular responses: proliferation or migration. The human organism has its own direction of life, but cancer deviates from the script to follow one of its own, upsetting the balance. Interfering with the communication that causes this deviation would be an innovative and promising therapeutic strategy”.
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