ArticleBreast cancer (Dove Medical Press)2023
CD24 May Serve as an Immunotherapy Target in Triple-Negative Breast Cancer by Regulating the Expression of PD-L1.
Article in Breast cancer (Dove Medical Press), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Fast-Food Component-Induced Epigenetic Modifications Modulate Immunotherapy in Metastatic Breast Cancer.ACS omega · 2026Article
- CD24 as an innate immune checkpoint in solid tumors: biology, biomarker stratification, and therapeutic translation.Frontiers in immunology · 2026Review
- Bioinformatics-based multi-omics and machine learning analysis identifies stemness-associated molecular subtypes and a prognostic index in breast cancer.Translational cancer research · 2025Article
- Targeting "don't eat me" signal: breast cancer immunotherapy.Breast cancer research and treatment · 2025Review
- The prognostic value of the tumor-stroma ratio compared to tumor-infiltrating lymphocytes in triple-negative breast cancer: a review.Virchows Archiv : an international journal of pathology · 2025Review
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: CD24 mediates a "don't eat me" signal to escape the immune environment. However, the correlation between CD24 and PD-L1 is unclear. This study aimed to assess if CD24 can serve as a target for immunotherapy of triple-negative breast cancer (TNBC). Methods: Data on CD24 expression in breast cancer were acquired using the Oncomine and UALCAN tools. The role of CD24 expression on the prognosis of patients with TNBC was assessed using Kaplan-Meier analyses. Subsequently, STRING and TISIDB databases were used to construct protein-protein interaction networks and to explore immune-related molecules regulated by CD24. Immunofluorescence and immunohistochemistry assays were conducted to validate CD24 and PD-L1 expression and tumor infiltration lymphocyte (TIL) level. Survival analysis was also performed to explore the effect of CD24 and PD-L1 expression and TIL level in patients with TNBC. ShRNA was also used to explore the regulation role of CD24 on PD-L1 expression. Results: CD24 expression was significantly higher in breast cancer than in normal tissues, with high expression being significantly associated with a worse prognosis. CD24 was found to be significantly regulated by chemokines, immunoinhibitors, immunostimulators and TILs. Furthermore, CD24 expression showed a significant positive correlation with PD-L1 expression and a negative correlation with TIL level. In association with PD-L1, CD24 was found to positively regulate lymphocyte costimulation, T cell costimulation, and leukocyte activation. Furthermore, CD24 and PD-L1 co-expression contributed to worse survival outcomes. In addition, CD24 expression was found to attenuate the positive effects of high-level TILs on the prognosis of patients with TNBC. CD24 can also regulate the expression of PD-L1 in TNBC cells. Conclusion: CD24 may attenuate the positive effects of high TIL levels on survival and may facilitate the immune escape of TNBC by regulating PD-L1 expression. Thus, it is a potential target for immunotherapy in TNBC.
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