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.
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Authors | Jin-Xia Wu, Feng-Xiao Shan, Jun-Nian Zheng, Dong-Sheng Pei |
Journal | Asian Pacific journal of cancer prevention : APJCP
(Asian Pac J Cancer Prev)
Vol. 15
Issue 2
Pg. 1041-6
( 2014)
ISSN: 2476-762X [Electronic] Thailand |
PMID | 24568448
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Arrestins
- Biomarkers, Tumor
- GABA type B receptor, subunit 1
- Receptors, GABA-B
- beta-Arrestins
- JNK Mitogen-Activated Protein Kinases
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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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