Oncotarget

Research Papers:

Overexpression of SYF2 promotes cell proliferation and correlates with poor prognosis in human breast cancer

Feng Shi, Feng-Feng Cai, Lu Cai, Xiao-Yan Lin, Wei Zhang, Qin-Qin Wang, Yu-Jie Zhao, Qi-Chao Ni, Hua Wang and Zhi-Xian He _

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Oncotarget. 2017; 8:88453-88463. https://doi.org/10.18632/oncotarget.18188

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Abstract

Feng Shi1,*, Feng-Feng Cai2,*, Lu Cai2, Xiao-Yan Lin2, Wei Zhang1, Qin-Qin Wang1, Yu-Jie Zhao1, Qi-Chao Ni1, Hua Wang1 and Zhi-Xian He1

1Department of General Surgery, Affiliated Hospital of Nantong University, Nantong University, Nantong, PR China

2Department of Breast Surgery, Yangpu Hospital, Tongji University School of Medicine, Shanghai, PR China

*These authors contributed equally to this work

Correspondence to:

Zhi-Xian He, email: hezhixian@ntu.edu.cn

Hua Wang, email: 13706292250@163.com

Keywords: SYF2, breast cancer, proliferation, prognosis

Received: January 10, 2017     Accepted: March 30, 2017     Published: May 23, 2017

ABSTRACT

SYF2, a known cell cycle regulator, is reported to be involved in cell cycle arrest by interacting with cyclin-D-type binding protein 1. In the present study, we investigated the role of SYF2 in human breast cancer (BC) progression. SYF2 was highly upregulated in BC tissues and cell lines, as per Western blot and immunohistochemistry analysis. The SYF2 expression level had a significant correlation with the tumor grade and Ki-67 expression. In vitro starvation-refeeding experiment and SYF2-siRNA transfection assay demonstrated that SYF2 could promote proliferation of BC cells, while SYF2 knockdown resulted in cells cycle arrest at G1/S phase, reducing the cell growth rate of BC cells. These results indicated that SYF2 promotes human BC progression by accelerating the BC cells’ proliferation. SYF2 could be a novel therapeutic target in human BC therapies.


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