Centro di Ricerca in Medicina Sperimentale (CERMS), Torino | Italy
We have shown that that miR-206, a microRNA responsible for downregulating the Met receptor during myogenesis, can push rhabdomyosarcoma (RMS) cells to resume differentiation, thus blocking tumor growth in xenograft models of RMS. Our current work is centered on the identification of other critical targets of miR-206, in the aim of developing a novel non-toxic approach to the treatment of RMS, a pediatric cancer often metastatic at diagnosis.
Keywords: Receptor tyrosine kinases / growth factor receptor signalling / RTKs in cancer / rhabdomyosarcoma / microRNAs
Subject area(s): Differentiation & Death | Molecular Medicine | Signal Transduction