期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 530, 期 1, 页码 122-129出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2020.07.015
关键词
Epithelial-mesenchymal transition; Invasion; TOPK; TGF-beta 1; NF-kappa B; Snail
资金
- National Research Foundation of Korea [NRF-2019R1I1A3A01063191]
- Priority Research Centers Program [NRF-2017R1A6A1A03015713]
TGF-beta 1 is known to induce epithelial-mesenchymal transition (EMT), which is a prerequisite for cancer cell invasion. Here we reveal that TOPK upregulates EMT and invasion of human breast cancer MDA-MB-231 or Hs578T cells via NF-kappa B-dependent Snail/Slug in TGF-beta 1 signaling. Endogenous TOPK expression was significantly increased in response to TGF-beta 1 and TOPK knockdown mitigated TGF-beta 1-induced breast cancer cell invasion. Interestingly, TOPK knockdown restored TGF-beta 1 suppression of E-cadherin expression and markedly reduced N-cadherin induced by TGF-beta 1. Also, NF-kappa B activity or expression of EMT markers Snail and Slug induced by TGF-beta 1 was decreased by TOPK knockdown. Meanwhile, knockdown of Snail or TOPK attenuated TGF-beta 1-induced breast cancer cell invasion. Taken, we conclude that TOPK mediates TGF-beta 1-induced EMT and invasion in breast cancer cells via NF-kappa B/Snail signaling, suggesting novel role of TOPK as therapeutic target in TGF-beta 1-mediated breast cancer development. (C) 2020 Elsevier Inc. All rights reserved.
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