#IDIBELLseminars: The Metabolic Dialogue Between Skeletal Muscle and Tumour

Skeletal muscle atrophy is a hallmark of cancer cachexia, an unmet medical need. Beyond being a passive victim of the disease, skeletal muscle is increasingly recognised as an active metabolic and endocrine organ, whose iron and heme handling shapes both local muscle integrity and systemic cancer progression. A central node of this crosstalk is the muscle-derived hormone erythroferrone (ERFE), induced in cachectic muscle. Locally, ERFE contributes to resistance to anabolic BMP-Smad signaling, favouring catabolism, while iron availability itself acts as a determinant of muscle function. Strikingly, skeletal muscle also behaves as an active driver of metastatic dissemination: muscle-specific deletion of the heme exporter FLVCR1a is sufficient to restrain metastatic spread, demonstrating that signals originating from muscle remotely influence cancer progression. This places muscle at the centre of a systemic axis coupling its metabolic state to tumour aggressiveness, and emerging as a therapeutic vulnerability in cancer

Hosted by Cristina Muñoz-Pinedo- Preclinical and experimental research in thoracic tumors (PReTT)

Paolo Ettore Porporato is Associate Professor of Experimental Biology at the University of Turin, where he leads the CaMeCa Lab (Cancer Metabolism and Cachexia) at the Molecular Biotechnology Center. After a PhD in Molecular Medicine and postdoctoral training at the Université catholique de Louvain in Pierre Sonveaux’s group, he returned to Italy in 2016 through the Rita Levi-Montalcini programme to establish his own research team. His work investigates the metabolic crosstalk between muscle and tumour, aiming to break the vicious cycle that drives cachexia and muscle wasting, bridging mitochondrial metabolism, iron homeostasis and tumour progression