NDLI: Overexpression of SMARCA5 correlates with cell proliferation and migration in breast cancer.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jin, Quanxiu Mao, Xiaoyun Li, Bo Guan, Shu Yao, Fan Jin, Feng
Description	Author Affiliation: Jin Q ( Department of Surgical Oncology and Breast Surgery, First Affiliated Hospital of China Medical University, Shenyang, Liaoning, China, 110001.)
Abstract	SMARCA5 partners with RSF-1 to compose the RSF complex, which belongs to the ISWI family of chromatin remodelers. Recent studies referred that SMARCA5 was overexpressed in some malignant tumors. However, expression pattern and biological roles of SMARCA5 in breast cancer have not been examined. In the present study, we found that SMARCA5 was overexpressed in breast cancer specimens by immunohistochemistry. Significant association was observed between SMARCA5 overexpression and TNM stage (p = 0.0199), tumor size (p = 0.0066), high proliferation index (p = 0.0366), and poor overall survival (p = 0.0141). SMARCA5 overexpression also correlated with Rsf-1 expression levels (p = 0.0120). Furthermore, colony formation assay and Matrigel invasion assay showed that knockdown of SMARCA5 expression in MDA-MB-231 and MDA-MB-435s cell lines with high endogenous expression decreased cell proliferation and cell invasion. Flow cytometry showed knockdown of SMARCA5-arrested cell cycle. Further analysis of cell cycle and invasion-related molecules showed that SMARCA5 downregulated cyclin A, MMP2 expression and upregulated p21 expression. In conclusion, our study demonstrated that SMARCA5 was overexpressed in human breast cancers and correlated with poor prognosis. SMARCA5 contributes to breast cancer cell proliferation and invasion.
File Format	HTM / HTML
ISSN	10104283
Issue Number	3
Volume Number	36
e-ISSN	14230380
Journal	Tumor Biology
Language	English
Publisher	Springer
Publisher Date	2015-03-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Subject Keyword	Discipline Medicine__semicolon__oncology Adenosine Triphosphatases Biosynthesis Breast Neoplasms Metabolism Pathology Cell Movement Physiology Chromosomal Proteins, Non-histone Genetics Cell Cycle Cell Line, Tumor Cell Proliferation Chromatin Assembly And Disassembly Cyclin A Cyclin D1 Cyclin-dependent Kinase Inhibitor P21 Down-regulation Female Gene Expression Regulation, Neoplastic Humans Matrix Metalloproteinase 2 Neoplasm Invasiveness Nuclear Proteins Trans-activators Up-regulation Journal Article
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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