ArticlePharmaceutical research2026
Silencing CD24 Inhibits Proliferation, Migration, and Chemoresistance in Triple-Negative Breast Cancer Cells.
Article in Pharmaceutical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- CD24 as an innate immune checkpoint in solid tumors: biology, biomarker stratification, and therapeutic translation.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
purposeThe expression of CD24 is significantly higher in triple-negative breast cancer (TNBC) compared to estrogen receptor and progesterone receptor-positive (ER
methodsWe designed four CD24 siRNAs and evaluated their silencing efficiency and biological activity in TNBC cells using different methods. We also examined the impact of CD24 silencing on doxorubicin resistance and macrophage-mediated phagocytosis of TNBC cells.
resultsWe have identified a CD24 siRNA that exhibits potent silencing activity in TNBC cells, effectively inhibiting their proliferation, migration, and invasion. CD24 silencing also induces apoptosis of TNBC cells and arrests the cell cycle in the S phase. Moreover, silencing CD24 enhances the sensitivity of TNBC cells to doxorubicin and increases macrophage-mediated phagocytosis of TNBC cells.
conclusionsTargeting CD24 with siRNAs is a promising therapeutic strategy for TNBC and other cancers characterized by CD24 overexpression.
Indexed as
Identifiers
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Registered trials
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