siRNA-mediated suppression of synuclein γ inhibits MDA-MB-231 cell migration and proliferation by downregulating the phosphorylation of AKT and ERK

Jingsong He, Ni Xie, Jianbo Yang, Hong Guan, Weicai Chen, Huisheng Wu, Zishan Yuan, Kun Wang, Guojin Li, Jie Sun, Limin Yu

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

Purpose: Synuclein-γ (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 MTT 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.

Original languageEnglish (US)
Pages (from-to)200-206
Number of pages7
JournalJournal of Breast Cancer
Volume17
Issue number3
DOIs
StatePublished - Sep 1 2014

Bibliographical note

Publisher Copyright:
© 2014 Korean Breast Cancer Society. All rights reserved.

Keywords

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

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