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Involvement of β-arrestins in cancer progression.

Abstract
β-arrestins, including β-arrestin1 and β-arrestin2, are ubiquitous cytosolic proteins which localize in the cytoplasm and plasma membrane, initially be regarded as an potential character in G protein-coupled receptors (GPCR) desensitization, sequestration, and internalization. Besides, recent many studies increasingly revealed that β-arrestins served widely as versatile adapter proteins for scaffolding many intracellular signaling networks to modulate the strength and duration of signaling by diverse types of receptors and downstream kinases. As we known, the biologic and clinical behaviors of many tumors are largely determined by multiple molecular signal pathways. More recently, accumulating evidences established that β-arrestins got widely involved in many cancer developmental signaling events which responsible for tumor viability and metastasis, suggesting an impressive role of β-arrestins in tumor progression. Because of the regulation and biological output of β-arrestins is so complex, the role of β-arrestins in cancer development still remains enigmatic. However, the further understanding with the clinical prognosis and oncogenic potential of β-arrestins might facilitate the identification of diagnosis biomarkers and development of drug targets in cancer. In this article, we reviewed a comprehensive summary of the β-arrestins-mediated functions in human cancers.
AuthorsShanshan Hu, Di Wang, Jingjing Wu, Juan Jin, Wei Wei, Wuyi Sun
JournalMolecular biology reports (Mol Biol Rep) Vol. 40 Issue 2 Pg. 1065-71 (Feb 2013) ISSN: 1573-4978 [Electronic] Netherlands
PMID23076527 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Arrestins
  • Receptors, G-Protein-Coupled
  • beta-Arrestins
Topics
  • Animals
  • Arrestins (physiology)
  • Cell Transformation, Neoplastic (metabolism)
  • Disease Progression
  • Humans
  • Neoplasms (metabolism, pathology)
  • Receptors, G-Protein-Coupled (metabolism)
  • Signal Transduction
  • beta-Arrestins

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