Functional Redundancy between ?1 and ?3 Integrin in Activating the IR/Akt/mTORC1 Signaling Axis to Promote ErbB2-Driven Breast Cancer (Cell Reports)

Using a mouse model of ErbB2-driven breast cancer, Bui et al. demonstrate a functional redundancy between two integrin subunits, ?1 and ?3, during mammary tumorigenesis. Mechanistically, both extracellular matrix (ECM) and integrin receptors regulate insulin receptor (IR) activity to promote the Akt/mTORC1 signaling axis, a crucial pathway to malignant transformation.