606
Views
144
CrossRef citations to date
0
Altmetric
Review

Grb2 signaling in cell motility and cancer

, &
Pages 1021-1033 | Published online: 12 Jul 2008
 

Abstract

Background: Metastasis is the primary cause of death in most human cancers, and understanding the molecular mechanisms underpinning this multistep process is fundamental to identifying novel molecular targets and developing more effective therapies. Objective/methods: Here we review the role of growth factor receptor-bound protein 2 (Grb2) in cancer and specifically in metastasis-related processes, and summarize the development of anticancer therapeutics selectively targeting this adapter protein. Results/conclusion: Grb2 is a key molecule in intracellular signal transduction, linking activated cell surface receptors to downstream targets by binding to specific phosphotyrosine-containing and proline-rich sequence motifs. Grb2 signaling is critical for cell cycle progression and actin-based cell motility, and, consequently, more complex processes such as epithelial morphogenesis, angiogenesis and vasculogenesis. These functions make Grb2 a therapeutic target for strategies designed to prevent the spread of solid tumors through local invasion and metastasis.

Acknowledgments

We would like to thank Georgia Shaw for her help in creating the artwork in .

Log in via your institution

Log in to Taylor & Francis Online

PDF download + Online access

  • 48 hours access to article PDF & online version
  • Article PDF can be downloaded
  • Article PDF can be printed
USD 99.00 Add to cart

Issue Purchase

  • 30 days online access to complete issue
  • Article PDFs can be downloaded
  • Article PDFs can be printed
USD 1,049.00 Add to cart

* Local tax will be added as applicable

Related Research

People also read lists articles that other readers of this article have read.

Recommended articles lists articles that we recommend and is powered by our AI driven recommendation engine.

Cited by lists all citing articles based on Crossref citations.
Articles with the Crossref icon will open in a new tab.