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Involvement of β-arrestins in cancer progression

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An Erratum to this article was published on 01 December 2012

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.

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Abbreviations

GPCRs:

G protein coupled receptors

GRKs:

G protein-coupled receptor kinases

TGF-β:

Transforming growth factor β

MAPK:

Mitogen activated protein kineases

PI3 K:

Phosphati dylinosito 3 kinase

ERK:

Extracellular regulated protein kinases

NSCLC:

Non small cell lung cancer

TβRIII:

The type III TGF- β receptor

COX-2:

Cyclooxygenase-2

PGE2 :

Prostaglandin E2

EP4 :

Prostanoid receptor

E2F1:

E2F transcription factor 1

CXCR4:

Chemokine(C-X-C motif) receptor 4

EGFR:

Epithelial growth factor receptor

ETAR:

Endothelin A receptor

ET-1:

Endothelin-1

EMT:

Epithelia to mesenchynal transition

GSK-3β:

Glycogen synthase kinase 3β

TP-β:

Thromboxane receptor β

AR:

Androgen receptor

PSA:

Prostate specific antigen

LPA:

Lysopho sphatidic acid

LPA1-3:

The type 1-3 lysophosphatidic acid receptor

NES:

Nuclear export signal

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Acknowledgments

This work was supported by grants from National Natural Science Foundation of China (No. 30973543, No. 81173075), Specialized Research Fund for the Doctoral Program of Higher Education of China (No. 20113420120002), Natural Science Foundation of the Higher Education Institutions of Anhui Province (No. KJ2012A153).

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Correspondence to Wei Wei.

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Hu, S., Wang, D., Wu, J. et al. Involvement of β-arrestins in cancer progression. Mol Biol Rep 40, 1065–1071 (2013). https://doi.org/10.1007/s11033-012-2148-0

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