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Derailed endocytosis: an emerging feature of cancer.

Author information

Affiliations

  • 1. Department of Biological Regulation, The Weizmann Institute of Science, Rehovot 76100, Israel.
      Authors
    • Mosesson Y 1
    (1 author)

Nature reviews. Cancer, 01 Nov 2008, 8(11):835-850
https://doi.org/10.1038/nrc2521 PMID: 18948996 

Review

A comment on this article appears in "Mechanism of E-cadherin lysosomal degradation." Nat Rev Cancer. 2009 Feb;9(2):143; author reply 143.

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.

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Read article at publisher's site: https://doi.org/10.1038/nrc2521

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Funding 

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NCI NIH HHS (3)