ArticleEuropean journal of medical research2025
C-type lectin domain family 3 member B (CLEC3B) inhibits triple-negative breast cancer chemoresistance via inducing ferroptosis.
Article in European journal of medical research, 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
- Unveiling the Mysteries of CLEC3B: Physiological Roles, Pathological Impacts, and Research Gaps.Cells · 2026Review
- CLEC3B (tetranectin) expression is associated with vascular localization and tumor aggressiveness in breast cancer.International journal of medical sciences · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
BACKGROUND AND
aimsCisplatin is one of effect chemotherapeutic drugs for triple-negative breast cancer (TNBC). However, cisplatin chemoresistance often generate in a notable proportion of TNBC patients, leading therapeutic failure. Thus, identification of key regulatory mechanisms for chemoresistance is important. Here, we aimed to study the functions and regulatory mechanisms of CLEC3B in cisplatin chemoresistance in TNBC.
methodsMTT assay, colony formation assay and Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay were employed to investigate the role of CLEC3B in cisplatin (CDDP) resistance in TNBC. Fe2
resultsHere, we find that CLEC3B was downregulated in TNBC tissues, especially in relapsed TNBC tissues. TNBC patients with high CLEC3B levels had better prognosis than those with low CLEC3B levels after chemotherapy. Functional assays showed that CLEC3B promoted CDDP chemosensitivity. Mechanistic assays found that CLEC3B promoted CDDP chemosensitivity via inducing ferroptosis. Moreover, CLEC3B interacted with SLC39A8 and SLC39A14 and knockdown of them reversed the effect of CLEC3B overexpression on chemosensitivity.
conclusionsIn summary, CLEC3B promotes chemosensitivity via interacting with SLC39A8 and SLC39A14 to induce ferroptosis.
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