ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Targeting ZNF570 activates ferroptosis to reverse tamoxifen resistance in ER + breast cancer cells.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Ferroptosis in breast cancer: From adipocyte-immune-iron regulation to therapeutic application.Clinical and translational medicine · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
The hormone receptors (HR) + /human epidermal growth factor receptor 2 (HER2) - subtype accounts for 60%-70% of primary breast cancer (BC) cases. Tamoxifen (TAM) has been the first-line endocrine therapeutic agent for this subtype for over 30 years and induces clinical responses in more than 70% of estrogen receptor-positive (ER +) tumors. However, 22%-52% of patients develop tumor recurrence or distant metastasis due to acquired tamoxifen resistance, which highlights the critical need to explore resistance mechanisms as well as identify new therapeutic targets for improving patient prognosis. The objective is to examine the role of ZNF570 in tamoxifen resistance of ER + BC. Analyses of The Cancer Genome Atlas (TCGA) database coupled with validation with clinical samples indicated that ZNF570 is overexpressed in HR + BC. Importantly, ZNF570 expression is linked to a poorer patient prognosis and serves as an independent prognostic indicator for HR + BC. Furthermore, ZNF570 expression is significantly higher in tumor tissues from tamoxifen-resistant patients than in those from tamoxifen-sensitive patients. Tamoxifen-resistant cell models (MCF7-TAM and T47D-TAM) were established by continuously exposing MCF-7 and T47D cells to tamoxifen for induction. These models demonstrated that ZNF570 expression is higher in resistant cells than their parental counterparts, and this expression level exhibits a positive link with estrogen receptor alpha (ERα) expression levels. Functional experiments demonstrated that ZNF570 knockout in tamoxifen-resistant cells significantly increased the cells' sensitivity to tamoxifen and reduced ER expression. Conversely, ZNF570 overexpression in parental MCF-7 as well as T47D cells decreased cells' sensitivity to tamoxifen and increased ER expression. Furthermore, ZNF570 was found to promote proliferation, invasion, and migration of ER + BC cells. Tumor-promoting effect of ZNF570 in vivo was validated by nude mouse xenograft experiments. Mechanistically, proteomic analyses and combined in vitro as well as in vivo experiments verified that ZNF570 knockout reverses tamoxifen resistance by activating ferroptosis. This ferroptosis activation is mediated by downregulating the expression of glutathione peroxidase 4 (GPX4) coupled with cystine/glutamate transporter (XCT), upregulating the expression of tumor protein p53 (TP53), rising intracellular levels of reactive oxygen species (ROS), ferrous ions (Fe
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