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CTCF negatively regulates HOXA10 expression in breast cancer cells

Authors
 Muhammad Mustaf  ;  Ji-Yeon Lee  ;  Myoung Hee Kim 
Citation
 Biochemical and Biophysical Research Communications, Vol.467(4) : 828-834, 2015 
Journal Title
 Biochemical and Biophysical Research Communications 
ISSN
 0006-291X 
Issue Date
2015
Abstract
HOX genes not only play important roles in defining body patterning during embryonic development, but also control numerous cellular events in adult cells. Deregulated HOX gene expression in different cancers including breast cancer is now increasingly being reported. Given that human HOXA cluster is marked with several CTCF binding sites, we investigated whether the presence of CTCF is associated directly with expression of HOXA genes in breast cancer cells. Several HOX genes, such as HOXA4, HOXA5 and HOXA10, were deregulated by CTCF overexpression and knockdown in MCF-7 cells. Among these genes, HOXA10 is an emerging tumor suppressor for its role in activation of p53 and in countering tumorigenesis in breast cancer. Here we provided evidences that CTCF functions as a negative regulator of HOXA10 in breast cancer cells. The putative promoter region of HOXA10 lies between 5.3 and 6.1 kb upstream of its start codon and its promoter activity was negatively regulated by CTCF. Together with in-silico analysis and in vitro mutation assay we identified a 20 bp CTCF binding motif flanking with core promoter element of HOXA10. HOXA10 promoter region was kept inactivated by maintaining H3K27me3 inactivation marks in the presence of CTCF. Epigenetic silencing of HOXA10 by CTCF in breast cancer cells may contribute towards tumorigenesis by decreasing apoptosis and promoting metastasis.
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/141820
DOI
10.1016/j.bbrc.2015.10.058
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실)
Yonsei Authors
김명희(Kim, Myoung Hee) ; 무하마드무스타파(Mustaf, Muhammad) ; 이지연(Lee, Ji Yeon)
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Full Text
http://www.sciencedirect.com/science/article/pii/S0006291X15307579
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