Abstract |
We report for the first time that Guanine nucleotide- binding protein subunit beta-2-like 1 (RACK1) formed a complex with Annexin A7. Hca-F and Hca-P are a pair of syngeneic mouse hepatocarcinoma cell lines established and maintained in our laboratory. Our previous study showed that both Annexin A7 and RACK1 were expressed higher in Hca-F ( lymph node metastasis >70%) than Hca-P ( lymph node metastasis <30%). Suppression of Annexin A7 expression in Hca-F cells induced decreased migration and invasion ability. In this study, knockdown of RACK1 by RNA interference (RNAi) had the same impact on metastasis potential of Hca-F cells as Annexin A7 down-regulation. Furthermore, by co-immunoprecipitation and double immunofluorescence confocal imaging, we found that RACK1 was in complex with Annexin A7 in control cells, but not in the RACK1-down-regulated cells, indicating the abolishment of RACK1-Annexin A7 interaction in Hca-F cells by RACK1 RNAi. Taken together, these results suggest that RACK1-Annexin A7 interaction may be one of the means by which RACK1 and Annexin A7 influence the metastasis potential of mouse hepatocarcinoma cells in vitro.
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Authors | Yue Du, Jinyi Meng, Yuhong Huang, Jun Wu, Bo Wang, Mohammed M Ibrahim, Jianwu Tang |
Journal | Biochemical and biophysical research communications
(Biochem Biophys Res Commun)
Vol. 445
Issue 1
Pg. 58-63
(Feb 28 2014)
ISSN: 1090-2104 [Electronic] United States |
PMID | 24491534
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2014 Elsevier Inc. All rights reserved. |
Chemical References |
- Annexin A7
- Neuropeptides
- RACK1 protein, mouse
- Receptors for Activated C Kinase
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Topics |
- Animals
- Annexin A7
(genetics, metabolism)
- Blotting, Western
- Carcinoma, Hepatocellular
(genetics, metabolism, pathology)
- Cell Line, Tumor
- Cell Movement
(genetics)
- Cell Proliferation
- Gene Expression Regulation, Neoplastic
- Liver Neoplasms
(genetics, metabolism, pathology)
- Lymphatic Metastasis
- Mice
- Microscopy, Confocal
- Neuropeptides
(genetics, metabolism)
- Protein Binding
- RNA Interference
- Receptors for Activated C Kinase
- Reverse Transcriptase Polymerase Chain Reaction
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