4.1 Article

siRNA-Mediated Suppression of Synuclein γ Inhibits MDA-MB-231 Cell Migration and Proliferation by Downregulating the Phosphorylation of AKT and ERK

期刊

JOURNAL OF BREAST CANCER
卷 17, 期 3, 页码 200-206

出版社

KOREAN BREAST CANCER SOC
DOI: 10.4048/jbc.2014.17.3.200

关键词

Breast neoplasms; Extracellular signal-regulated MAP kinases; Human SNCG protein; Proto-oncogene proteins c-akt; Small interfering RNA

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资金

  1. Basic Research Program for Scientific and Technological Innovation of Shenzhen City [JC201105170637, JCYJ20130329110955809, JCYJ20120613171430264]
  2. Key Program for Science and Technology of Shenzhen City [201101005]
  3. International Joint Program for Scientific and Technological Innovation of Shenzhen City [GJHZ20120614154716498, GJHZ20130412153906740]

向作者/读者索取更多资源

Purpose: Synuclein-gamma (SNCG), which was initially identified as breast cancer specific gene 1, is highly expressed in advanced breast cancers, but not in normal or benign breast tissue. This study aimed to evaluate the effects of SNCG siRNA-treatment on breast cancer cells and elucidate the associated mechanisms. Methods: Vectors containing SNCG and negative control (NC) siRNAs were transfected into MDA-MB-231 cells; mRNA levels were determined by real-time polymerase chain reaction. Cell proliferation was evaluated using the MU assay, cell migration was assessed by the Transwell assay, apoptosis and cell cycle analyses Were conducted with the flow cytometer, and Western blot analysis was performed to determine the relative levels of AKT, ERK, p-AKT, and p-ERK expression. Results: SNCG mRNA levels were significantly reduced in MDA-MB-231 cells transfected with SNCG siRNA. Our results indicate that in SNCG siRNA-treated cells, cell migration and proliferation decreased significantly, apoptosis was induced, and the cell cycle was arrested. Western blot analysis indicated that the protein levels of p-AKT and p-ERK were much lower in the SNCG siRNA-treated groups, than in the control and NC groups. Conclusion: SNCG siRNA could decrease the migration and proliferation of breast cancer cells by downregulating the phosphorylation of AKT and ERK.

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