Dimerización de ERK como determinante de factores de progresión tumoral

Abstract

Nearly 50% of human malignancies have dysregulated RAS-ERK signalling; inhibiting it is a valid strategy for antineoplastic intervention. ERK dimerization is essential for extranuclear ERK signalling, but not for nuclear signalling. Here we describe the role of ERK dimers in tumour progression in response to different stimuli. ERK dimerization-mediated cell spreading involves actin remodelling and ERK scaffold proteins as potential targets driven during tumorigenesis. In this study, we performed chemotaxis assays and employed 2D migration, 3D organoid formation and chick embryo metastasis models. We have observed the tumorigenic role mediated by ERK dimerization at different stages of tumour progression, monitored with the ERK dimer inhibitor DEL-22379.