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Am J Physiol Endocrinol Metab 296: E973-E984, 2009. First published February 24, 2009; doi:10.1152/ajpendo.90857.2008
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REVIEWS

Breakdown of endocytosis in the oncogenic activation of receptor tyrosine kinases

Jasmine V. Abella1,4 and Morag Park1,2,3,4

Departments of 1Biochemistry, 2Medicine, and 3Oncology; and 4Molecular Oncology Group, McGill University, Montreal, Quebec, Canada

Submitted 23 February 2008 ; accepted in final form 16 February 2009

ABSTRACT

There is increasing evidence to support the concept that the malignant behavior of many tumors is sustained by the deregulated activation of growth factor receptors. Activation of receptor tyrosine kinases (RTKs) by their respective ligand(s) initiates cellular signals that tightly modulate cell proliferation, survival, differentiation and migration to ensure normal tissue patterning. Therefore, uncontrolled activation of such signals can have deleterious effects, leading to oncogenesis. To date, deregulation of most RTKs has been implicated in the development of cancer, although the mechanisms that lead to their deregulation are not yet fully understood (10). RTK endocytosis, the internalization and trafficking of receptors inside the cell, has long been established as a mechanism to attenuate RTK signaling. However, RTKs have been demonstrated to continue to signal along the endocytic pathway, which contributes to the spatio-temporal regulation of signal transduction. This review will focus on recent advances linking defective endocytosis of RTKs in the development of cancer.

Cbl; ubiquitination; receptor downregulation


Address for reprint requests and other correspondence: M. Park, Rosalind and Morris Goodman Cancer Centre, Rm. 511, 1160 Pine Ave West, Montreal, H3A 1A3, QC, Canada (e-mail: morag.park{at}mcgill.ca)






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