TY - JOUR
T1 - Derailed endocytosis
T2 - An emerging feature of cancer
AU - Mosesson, Yaron
AU - Mills, Gordon B.
AU - Yarden, Yosef
N1 - Funding Information:
We thank Y. Zwang and T. Goldkorn for insightful comments. Y.Y. is the incumbent of the Harold and Zelda Goldenberg Professorial Chair. His laboratory is supported by research grants from the U.S. National Cancer Institute (NCI; CA072981), the Israel Science Foundation, Dr. Miriam and Sheldon G. Adelson Medical Research Foundation and the German–Israeli Foundation. G.B.M. is supported by the Komen Foundation and the NCI (PO1CA099031).
PY - 2008/11
Y1 - 2008/11
N2 - 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.
AB - 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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U2 - 10.1038/nrc2521
DO - 10.1038/nrc2521
M3 - Review article
C2 - 18948996
AN - SCOPUS:54549102284
SN - 1474-175X
VL - 8
SP - 835
EP - 850
JO - Nature Reviews Cancer
JF - Nature Reviews Cancer
IS - 11
ER -