Abstract

Once engaged by soluble or matrix-anchored ligands, cell surface proteins are commonly sorted to lysosomal degradation through several endocytic pathways. Defective vesicular trafficking of growth factor receptors, as well as unbalanced recycling of integrin- and cadherin-based adhesion complexes, has emerged in the past 5 years as a multifaceted hallmark of malignant cells. In line with the cooperative nature of endocytic machineries, multiple oncogenic alterations underlie defective endocytosis, such as altered ubiquitylation (Cbl and Nedd4 ubiquitin ligases, for example), altered cytoskeletal interactions and alterations to Rab family members. Pharmaceutical interception of the propensity of tumour cells to derail their signalling and their adhesion receptors may constitute a novel target for cancer therapy.

Author affiliations

1. Department of Biological Regulation, The Weizmann Institute of Science, Rehovot 76100, Israel
2. Department of Systems Biology, MD Anderson Cancer Center, Houston, Texas 77030, USA.

Correspondence to: Yosef Yarden¹ Email: yosef.yarden@weizmann.ac.il

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