ArticleCancer science2025
PSMD14/E2F1 Axis-Mediated CENPF Promotes the Metastasis of Triple-Negative Breast Cancer Through Inhibiting Ferroptosis.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Targeting PSMD14 enhances immunotherapy efficacy by promoting PD-L1 degradation and reshaping the tumor microenvironment in breast cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- FOXM1 Signaling Network Transcriptionally Upregulates Expression of Proteins Involved in Mitotic Progression to Induce High Proliferation and Chromosomal Instability in Androgen Receptor-Low Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- Identification ofFrontiers in pharmacology · 2026Article
- PSMD14 as a translational target in cancer and beyond: from deubiquitination mechanisms to drug resistance and precision therapy.Cancer drug resistance (Alhambra, Calif.) · 2026Review
- Article
- PSMD14 drives lung adenocarcinoma progression through HMMR stabilization and dual activation of TGF-β/Smad and PI3K/AKT/mTOR signaling.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The metastasis of triple-negative breast cancer (TNBC) usually contributes to the failure of treatment. Centromere Protein F (CENPF) can induce proliferation and metastasis in TNBC. Nevertheless, the upstream mechanism of CENPF in BC remains unclear. Western blot and RT-qPCR were employed for testing the levels of PSMD14, E2F1, and CENPF, and cell migration was assessed using the Transwell assay. Additionally, the CCK8 assay was applied to investigate cell viability, and C11-BODIPY 581/591 was applied to assess the lipid ROS level. ChIP and dual luciferase assays were used to examine the association between E2F1 and the CENPF promoter. The interaction between PSMD14 and E2F1 was verified using Co-IP. Knockdown of CENPF could significantly inhibit migration and invasion in TNBC cells. In addition, the silencing of CENPF aggravated arachidonic acid metabolism-induced ferroptosis in TNBC cells. Meanwhile, E2F1 knockdown greatly inhibited the expressions of CENPF and attenuated TNBC cell invasion and migration by decreasing its binding with the CENPF promoter. More importantly, PSMD14 could suppress arachidonic acid metabolism-induced ferroptosis in TNBC cells through the E2F1/CENPF axis. The PSMD14/E2F1 axis-mediated CENPF could promote the metastasis of TNBC by inhibiting arachidonic acid metabolism-induced ferroptosis. This research might bring novel insights into discovering methods for alleviating tumor metastasis in TNBC.
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Registered trials
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