BMB Reports 2019; 52(2): 139-144  https://doi.org/10.5483/BMBRep.2019.52.2.235
SETDB1 regulates SMAD7 expression for breast cancer metastasis
Tae Young Ryu1,#, Kwangho Kim1,#, Seon-Kyu Kim1, Jung-Hwa Oh3, Jeong-Ki Min1,2, Cho-Rok Jung1,2, Mi-Young Son1,2, Dae-Soo Kim1,2,* and Hyun-Soo Cho1,2,*
1Korea Research Institute of Bioscience and Biotechnology, 2Department of Functional Genomics, Korea University of Science and Technology, Daejeon 34141, 3Korea Institute of Toxicology (KIT), Daejeon 34114, Korea
Correspondence to: Hyun-Soo Cho, Tel: +82-42-879-8152; Fax: +82-42-860-4608; E-mail: chohs@kribb.re.kr; Dae-Soo Kim, Tel: +82-42-879-8291; Fax: +82-42-879-8139; E-mail: kds2465@kribb.re.kr
#These authors contributed equally to this work.
Received: October 5, 2018; Revised: October 8, 2018; Accepted: December 3, 2018; Published online: February 28, 2019.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

cc This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Breast cancer (BRC) is the most invasive cancer in women. Although the survival rate of BRC is gradually increasing due to improved screening systems, development of novel therapeutic targets for inhibition of BRC proliferation, metastasis and recurrence have been constantly needed. Thus, in this study, we identified overexpression of SETDB1 (SET Domain Bifurcated 1), a histone methyltransferase, in RNA-seq data of BRC derived from TCGA portal. In Gene Ontology (GO) analysis, cell migration-related GO terms were enriched, and we confirmed down-regulation of cell migration/invasion and alteration of EMT /MET markers after knockdown of SETDB1. Moreover, gene network analysis showed that SMAD7 expression is regulated by SETDB1 levels, indicating that up-regulation of SMAD7 by SETDB1 knockdown inhibited BRC metastasis. Therefore, development of SETDB1 inhibitors and functional studies may help develop more effective clinical guidelines for BRC treatment.
Keywords: Breast cancer, Metastasis, SETDB1


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