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Functional roles of CTCF in breast cancer
( Sumin Oh ),( Chaeun Oh ),( Kyung Hyun Yoo ) 생화학분자생물학회(구 한국생화학분자생물학회) 2017 BMB Reports Vol.50 No.9
CTCF, Zinc-finger protein, has been identified as a multifunctional transcription factor that regulates gene expression through various mechanisms, including recruitment of other co-activators and binding to promoter regions of target genes. Furthermore, it has been proposed to be an insulator protein that contributes to the establishment of functional threedimensional chromatin structures. It can disrupt transcription through blocking the connection between an enhancer and a promoter. Previous studies revealed that the onset of various diseases, including breast cancer, could be attributed to the aberrant expression of CTCF itself or one or more of its target genes. In this review, we will describe molecular dysfunction involving CTCF that induces tumorigenesis and summarize the functional roles of CTCF in breast cancer. [BMB Reports 2017; 50(9): 445-453]
E1A physically interacts with RUNX3 and inhibits its transactivation activity
Cha, Eun‐,Jeong,Oh, Byung‐,Chul,Wee, Hee‐,Jun,Chi, Xin‐,Zi,Goh, Yun‐,Mi,Lee, Kyeong‐,Sook,Ito, Yoshiaki,Bae, Suk‐,Chul Wiley Subscription Services, Inc., A Wiley Company 2008 Journal of cellular biochemistry Vol.105 No.1
<P><B>Abstract</B></P><P>The adenoviral gene, termed <I>early region 1A</I> (<I>E1A</I>), is crucial for transformation and has been used very effectively as a tool to determine the molecular mechanisms that underlie the basis of cellular transformation. pRb, p107, p130, p300/CBP, p400, TRRAP, and CtBP were identified to be E1A‐binding proteins and their roles in cellular transformation have been established. Although the major function of E1A is considered to be the regulation of gene expression that is critical for differentiation and cell cycle exit, one of the most significant questions relating to E1A transformation is how E1A mediates this regulation. RUNX3 is a transcription factor that was first described as a gastric cancer tumor suppressor but is now known to be involved in many different cancers. Exogenous expression of <I>RUNX3</I> strongly inhibits the growth of cells. Here, we show that the adenovirus oncoprotein E1A interacts with RUNX3 in vitro and in vivo. RUNX3 interacts with the N‐terminus (amino acids 2‐29) of E1A, which is known to interact with p300/CBP, p400, and TRRAP. E1A interacts directly with the Runt domain of RUNX3 but does not interfere with CBFβ‐RUNX3 interactions. In addition, E1A inhibits the transactivation activity of RUNX3 on the <I>p21</I><SUP><I>WAF1/CIP1</I></SUP> promoter. Consistent with these observations, the growth inhibition induced by RUNX3 is reduced by E1A. These results demonstrate that E1A specifically binds to RUNX3 and inactivates its transactivation activity. We propose that one of the mechanisms for the oncogenic activity of E1A is the inhibition of RUNX3, similar to that of RB and p300/CBP. J. Cell. Biochem. 105: 236–244, 2008. © 2008 Wiley‐Liss, Inc.</P>