Open AccessSETDB1 regulates SMAD7 expression for breast cancer metastasis
Author(s) -
Tae Young Ryu,
KwangHo Kim,
SeonKyu Kim,
JungHwa Oh,
JeongKi Min,
ChoRok Jung,
MiYoung Son,
DaeSoo Kim,
HyunSoo Cho
Publication year - 2019
Publication title -
bmb reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.511
H-Index - 77
eISSN - 1976-670X
pISSN - 1976-6696
DOI - 10.5483/bmbrep.2019.52.2.235
Subject(s) - breast cancer , metastasis , cancer research , breast cancer metastasis , oncology , expression (computer science) , medicine , cancer , biology , cancer metastasis , computer science , programming language
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.
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