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Biochem Biophys Res Commun. 2018 Apr 6;498(3):509-515. doi: 10.1016/j.bbrc.2018.03.011. Epub 2018 Mar 3.

ELK3-GATA3 axis modulates MDA-MB-231 metastasis by regulating cell-cell adhesion-related genes.

Author information

1
Department of Biomedical Science, College of Life Science, CHA University, Seongnam, South Korea.
2
Digestive Disease Center, CHA Bundang Medical Center, CHA University, Seongnam, South Korea. Electronic address: mykim@cha.ac.kr.
3
Department of Biomedical Science, College of Life Science, CHA University, Seongnam, South Korea. Electronic address: kspark@cha.ac.kr.

Abstract

GATA3 is a master regulator that drives mammary epithelial cell differentiation, and the suppression of GATA3 expression is associated with the development of aggressive breast cancer. However, the mechanism through which GATA3 loss drives cancer development is poorly understood. Previously, we reported that ELK3 suppression in MDA-MB-231 (ELK3 KD) resulted in the reprogramming of these cells from a basal to luminal subtype, which was associated with the induction of GATA3 expression, and that the ELK3-GATA3 axis orchestrated the metastatic characteristics of MDA-MB-231. Here, we show that GATA3 suppression in ELK3 knockdown MDA-MB-231 cells (ELK3/GATA3 DKD) restores the metastatic ability comparably to that of control MDA-MB-231 cells, even though the epithelial cell morphology and TGF-β signaling of ELK3 KD are not recovered in ELK3/GATA3 DKD. The expression of E-cadherin and tight junctional proteins, including occludin, claudin and ZO-1, which is activated in ELK3 KD, is suppressed in ELK3/GATA3 DKD. These results reveal the possibility that the ELK3-GATA3 axis determines the metastatic characteristics of MDA-MB-231 by regulating the expression of cell-cell adhesion factors.

KEYWORDS:

E-cadherin; GATA3; Lung metastasis; Tight junction

PMID:
29510139
DOI:
10.1016/j.bbrc.2018.03.011
[Indexed for MEDLINE]

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