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β-arrestin promotes c-Jun N-terminal kinase mediated apoptosis via a GABA(B)R·β-arrestin·JNK signaling module.

Abstract
Evidence is growing that the GABAB receptor, which belongs to the G protein-coupled receptor (GPCR) superfamily, is involved in tumorigenesis. Recent studies have shown that β-arrestin can serve as a scaffold to recruit signaling protein c-Jun N-terminal knase (JNK) to GPCR. Here we investigated whether β-arrestin recruits JNK to the GABAB receptor and facilitates its activation to affect the growth of cancer cells. Our results showed that β-arrestin expression is decreased in breast cancer cells in comparison with controls. β-arrestin could enhance interactions of the GABABR·β-arrestin·JNK signaling module in MCF-7 and T-47D cells. Further studies revealed that increased expression of β-arrestin enhances the phosphorylation of JNK and induces cancer cells apoptosis. Collectively, these results indicate that β-arrestin promotes JNK mediated apoptosis via a GABABR·β-arrestin·JNK signaling module.
AuthorsJin-Xia Wu, Feng-Xiao Shan, Jun-Nian Zheng, Dong-Sheng Pei
JournalAsian Pacific journal of cancer prevention : APJCP (Asian Pac J Cancer Prev) Vol. 15 Issue 2 Pg. 1041-6 ( 2014) ISSN: 2476-762X [Electronic] Thailand
PMID24568448 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Arrestins
  • Biomarkers, Tumor
  • GABA type B receptor, subunit 1
  • Receptors, GABA-B
  • beta-Arrestins
  • JNK Mitogen-Activated Protein Kinases
Topics
  • Apoptosis
  • Arrestins (metabolism)
  • Biomarkers, Tumor (metabolism)
  • Blotting, Western
  • Breast Neoplasms (metabolism, pathology)
  • Cell Proliferation
  • Female
  • Humans
  • Immunoprecipitation
  • JNK Mitogen-Activated Protein Kinases (metabolism)
  • Phosphorylation
  • Receptors, GABA-B (metabolism)
  • Signal Transduction
  • Tumor Cells, Cultured
  • beta-Arrestins

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