DNAJB9 suppresses the metastasis of triple-negative breast cancer by promoting FBXO45-mediated degradation of ZEB1

被引:37
作者
Kim, Hye-Youn [1 ]
Kim, Young-Mi [2 ]
Hong, Suntaek [1 ,2 ]
机构
[1] Gachon Univ, Lee Gil Ya Canc & Diabet Inst, Dept Biochem, Coll Med, Incheon 21999, South Korea
[2] Gachon Univ, Dept Hlth Sci & Technol, GAIHST, Incheon 21999, South Korea
基金
新加坡国家研究基金会;
关键词
EPITHELIAL-MESENCHYMAL TRANSITION; BETA-CATENIN; PROTEIN; HLJ1; EXPRESSION; TRANSCRIPTION; PROGRESSION; TARGET; HSP90; REGULATOR;
D O I
10.1038/s41419-021-03757-x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
DNAJB9, a member of the heat shock protein 40 family, acts as a multifunctional player involved in the maintenance of their client proteins and cellular homeostasis. However, the mechanistic action of DNAJB9 in human malignancies is yet to be fully understood. In this study, we found that ectopic restoration of DNAJB9 inhibits the migration, invasion, in vivo metastasis, and lung colonization of triple-negative breast cancer (TNBC) cells. Mechanistically, DNAJB9 stabilizes FBXO45 protein by suppressing self-ubiquitination and reduces the abundance of ZEB1 by Lys48-linked polyubiquitination to inhibit the epithelial-mesenchymal transition (EMT) and metastasis. Clinically, the reduction of DNAJB9 expression, concomitant with decreased FBXO45 abundance in breast cancer tissues, correlates with poorer clinical outcomes of patients with breast cancer. Taken together, our results provide a novel insight into the metastasis of TNBC and define a promising therapeutic strategy for cancers with overactive ZEB1 by regulating the DNAJB9-FBXO45 signaling axis.
引用
收藏
页数:12
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