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Synuclein-γ promotes migration of MCF7 breast cancer cells by activating extracellular-signal regulated kinase pathway and breaking cell-cell junctions

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Synuclein-γ (SNCG), a synuclein family member, promotes migration, invasion and metastasis of tumor cells; however, the mechanism remains unclear. The present study investigated the effect of SNCG on malignant phenotypes of MCF7 cells using cell proliferation analysis, cell migration assays and wound healing assays, and verified its effects on extracellularsignal regulated kinase (Erk) activation and epithelial to mesenchymal transitionrelated markers using western blotting. The results indicated that SNCG increased migration (P<0.05) but not proliferation (P=0.711) of MCF7 cells. It was also demonstrated that SNCG activated the Erk pathway and an inhibitor of Erk signaling significantly counteracted SNCGinduced migration. Furthermore, it was shown that SNCG downregulated levels of tight junctionsassociated factors Ecadherin and ZO1, while inhibiting the Erk pathway did not affect their levels. In conclusion, SNCG may promote MCF7 cell migration through activating the Erk pathway and breaking cell-cell junctions.

Document Type: Research Article

Affiliations: Department of Biochemistry and Molecular Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing 100142, P.R. China

Publication date: 01 September 2015

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  • Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
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