ArticleCell biochemistry and biophysics2025
DCTPP1 is Transcriptionally Activated by FOXA1 to Affect Cisplatin Sensitivity in Triple-Negative Breast Cancer via Suppression of Ferroptosis.
Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Ferroptosis in chemotherapy resistance and resensitization in breast cancer: a systematic review of preclinical evidence and translational implications.Frontiers in oncology · 2026Pooled it
- A Comprehensive Understanding ofCurrent issues in molecular biology · 2026Review
- Spatial transcriptome and single-cell sequencing reveal the role of nucleotide metabolism in breast cancer progression and tumor microenvironment.Frontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Triple negative breast cancer (TNBC) leads to significant global death due to the therapeutic failure such as the development of chemoresistance. The objective of this study was to discover the potential targets inhibiting cancer progression and enhancing cisplatin sensitivity in TNBC. Forkhead Box Protein A1 (FOXA1) and deoxycytidine triphosphate pyrophosphatase 1 (DCTPP1) expression was detected via real-time quantification PCR and western blotting. Cell proliferation and death were examined using EdU and flow cytometry. Transwell migration/invasion assays were performed to assess cell metastasis. Associated indicators were determined to evaluate ferroptosis. Half inhibitory concentration of cisplatin was tested via cell counting kit-8 assay. In vivo assays were implemented using xenograft models in mice. FOXA1 and DCTPP1 binding was validated through chromatin immunoprecipitation and dual-luciferase reporter assays. DCTPP1 was highly expressed in TNBC tissues and cells, and DCTPP1 was related to poor prognosis. Silencing DCTPP1 impeded TNBC cell malignant phenotypes (reduced proliferation, inhibited migration/invasion, and enhanced cell death) in vitro and tumor growth in vivo. DCTPP1 knockdown increased cisplatin sensitivity of TNBC cells via inducing ferroptosis. FOXA1 activated transcription of DCTPP1 and then promoted DCTPP1 expression. FOXA1 overexpression contributed to TNBC cell development, while inhibited ferroptosis and cisplatin sensitivity. FOXA1 knockdown facilitated ferroptosis and cisplatin sensitivity by targeting DCTPP1 in TNBC cells. Animal model also showed that FOXA1/DCTPP1 mediated cisplatin sensitivity through ferroptosis in vivo. The above evidence elucidated the role of FOXA1-mediated DCTPP1 in regulating TNBC development and cisplatin sensitivity by mediating ferroptosis.
Indexed as
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.