A molecular mechanism for controlling breast cancer progression identified

The discovered mechanism presents a bidirectional nature: if on the one hand Shp1 counteracts the pro-tumor action, on the other hand interleukin 8 can chemically deactivate the Shp1 protein, triggering the destruction of the receptor through which the signal is transmitted. This dynamic indicates that the tumor is able to self-regulate its aggressiveness through a hitherto unknown receptor stability control system. As he explains Alessia Varone, Cnr-Ieomi researcher and coordinator of the study: “We have identified a completely new way in which tumor cells regulate IL-8 signaling. This mechanism opens the way to the study of similar processes also for other proteins crucial in the tumor environment“.

Data analysis revealed that this molecular pathway is particularly active in two subtypes of breast cancer that are complex to treat: luminal tumors and the so-called “triple negatives”. In the latter, the presence of low levels of Shp1 was associated with high IL-8 production and more critical prognosis, suggesting that monitoring this protein can act both as a diagnostic marker and as a target for future targeted therapeutic protocols.

The integration between public basic research and the experience of the pharmaceutical industry has made it possible to accelerate the transition from in vitro observations to the evaluation of possible medical applications. “Our data suggest that acting on this mechanism could represent an innovative strategy to combat the most aggressive tumors“, adds Daniela Corda, Cnr-Ieomi researcher and senior co-author of the work. “It is a concrete example of how collaboration between public research and the pharmaceutical industry can accelerate the transfer of knowledge towards clinical applications“.

Interleukin 8 also plays an important role in other solid tumors, such as those of the lung, pancreas and prostate.making this finding potentially applicable to a broader oncology context.