Guanine nucleotide-binding protein subunit beta-2-like 1, a new Annexin A7 interacting protein

• DOI: 10.1016/j.bbrc.2014.01.119
• Publication Date: 2014-02-02T16:31:31Z
• Authors: Yue Du; Jinyi Meng; Yuhong Huang; Jun Wu; Bo Wang; Mohammed M. Ibrahim; Jianwu Tang
• Keywords: 0301 basic medicine; Carcinoma, Hepatocellular; Microscopy, Confocal; Reverse Transcriptase Polymerase Chain Reaction; Blotting, Western; Liver Neoplasms; Neuropeptides; Receptors for Activated C Kinase; Gene Expression Regulation, Neoplastic; Mice; 03 medical and health sciences; Cell Movement; Cell Line, Tumor; Lymphatic Metastasis; Animals; Annexin A7; RNA Interference; Cell Proliferation; Protein Binding

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.