Model for endocytic transport of ERα and β1-integrin regulated by FN in breast cancer cells. Estrogens induce rapid endocytosis of membrane ERα–β1-integrin complexes, generating EEA1⁺ vesicles. In the absence of FN, vesicles containing β1-integrin and ERα could either fuse to the nuclear membrane where ERα exerts its action or follow the lysosomal pathway, where ERα colocalizes with Rab7. After 60 min, ERα and β1-integrin are degraded in lysosomes and the signal ends. In the presence of FN, ERα and β1-integrin are localized in Rab11⁺ vesicles, suggesting that they might be recycled and therefore avoid the lysosomal pathway. ERα and β1-integrin levels are maintained over time and the cycle continues, keeping ERα transcriptionally active.