TY - JOUR
T1 - siRNA-mediated suppression of synuclein γ inhibits MDA-MB-231 cell migration and proliferation by downregulating the phosphorylation of AKT and ERK
AU - He, Jingsong
AU - Xie, Ni
AU - Yang, Jianbo
AU - Guan, Hong
AU - Chen, Weicai
AU - Wu, Huisheng
AU - Yuan, Zishan
AU - Wang, Kun
AU - Li, Guojin
AU - Sun, Jie
AU - Yu, Limin
N1 - Publisher Copyright:
© 2014 Korean Breast Cancer Society. All rights reserved.
PY - 2014/9/1
Y1 - 2014/9/1
N2 - 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.
AB - 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.
KW - Breast neoplasms
KW - Extracellular signal-regulated MAP kinases
KW - Human SNCG protein
KW - Proto-oncogene proteins c-akt
KW - Small interfering RNA
UR - http://www.scopus.com/inward/record.url?scp=84923324107&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84923324107&partnerID=8YFLogxK
U2 - 10.4048/jbc.2014.17.3.200
DO - 10.4048/jbc.2014.17.3.200
M3 - Article
C2 - 25320617
AN - SCOPUS:84923324107
SN - 1738-6756
VL - 17
SP - 200
EP - 206
JO - Journal of Breast Cancer
JF - Journal of Breast Cancer
IS - 3
ER -