ArticleActa pharmacologica Sinica2022
Therapeutic efficacy and mechanism of CD73-TGFβ dual-blockade in a mouse model of triple-negative breast cancer.
Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 21 citations in OpenAlex.
- Breast Cancer Milieu Maneuvers Cancer-Associated Macrophages to Synergize Neoplastic Repertoires.Cancers · 2026Review
- Molecular and Immune Mechanisms Governing Cancer Metastasis, Including Dormancy, Microenvironmental Niches, and Tumor-Specific Programs.International journal of molecular sciences · 2026Review
- Potent Competitive Inhibitors of Ecto-5'-nucleotidase (CD73) based on 6‑(Het)aryl-7-deazapurine Ribonucleoside 5'‑ACS pharmacology & translational science · 2026Article
- Increased primary breast tumor expression of CD73 is associated with development of bone metastases and is a potential biomarker for adjuvant bisphosphonate use.Scientific reports · 2025Article
- Plasticity of myeloid-derived suppressor cells in cancer and cancer therapy.Oncology research · 2025Review
- Inflammation-associated drug resistance and tumor growth in TNBC.Frontiers in immunology · 2025Review
- CD73Frontiers in medicine · 2025Article
- [Myeloid-derived suppressor cells as important factors and potential targets for breast cancer progression].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Review
- Adenosine signaling in tumor-associated macrophages and targeting adenosine signaling for cancer therapy.Cancer biology & medicine · 2024Review
- Comprehensive pan-cancer analysis of CD73: Explore its association with prognosis and tumor immune microenvironment.Heliyon · 2024Article
- CD73 promotes non-small cell lung cancer metastasis by regulating Axl signaling independent of GAS6.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Pharmacological suppression of the OTUD4/CD73 proteolytic axis revives antitumor immunity against immune-suppressive breast cancers.The Journal of clinical investigation · 2024Article
- Current perspectives and trends of CD39-CD73-eAdo/A2aR research in tumor microenvironment: a bibliometric analysis.Frontiers in immunology · 2024Article
- Dynamic ultrasound molecular-targeted imaging of senescence in evaluation of lapatinib resistance in HER2-positive breast cancer.Cancer medicine · 2023Article
- The Clinical Significance of CD73 in Cancer.International journal of molecular sciences · 2023Review
- Tumor cell plasticity in targeted therapy-induced resistance: mechanisms and new strategies.Signal transduction and targeted therapy · 2023Review
- Unlocking molecular mechanisms and identifying druggable targets in matched-paired brain metastasis of breast and lung cancers.Frontiers in immunology · 2023Article
- CD73 regulates zoledronate-induced lymphocyte infiltration in triple-negative breast cancer tumors and lung metastases.Frontiers in immunology · 2023Article
- NT5E upregulation in head and neck squamous cell carcinoma: A novel biomarker on cancer-associated fibroblasts for predicting immunosuppressive tumor microenvironment.Frontiers in immunology · 2022Article
- CD73 (NT5E) Promotes the Proliferation and Metastasis of Lung Adenocarcinoma through the EGFR/AKT/mTOR Pathway.BioMed research international · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although chemotherapy and recently approved immunotherapies have improved treatment of triple-negative breast cancer (TNBC), the clinical outcome for this deadly disease remains unsatisfactory. We found that both cluster of differentiation 73 (CD73) and transforming growth factor (TGF)β were elevated in TNBC and correlated with the epithelial-mesenchymal transition (EMT), fibrotic stroma, an immune-tolerant tumor environment, and poor prognosis. To explore the efficacy of CD73-TGFβ dual-blockade, we generated a bifunctional anti-CD73-TGFβ construct consisting of the CD73 antibody MEDI9447 fused with the TGFβRII extracellular-domain (termed MEDI-TGFβR). MEDI-TGFβR retained full and simultaneous blocking efficiency for CD73 and TGFβ. Compared with MEDI9447 activity alone, MEDI-TGFβR demonstrated superior inhibitory activity against CD73-dependent cell migration and the EMT in CD73-high TNBC cells and effectively reduced lung metastasis in a syngeneic mouse model of TNBC. Mechanistically, the CD73-TGFβ dual-blockade reverted the EMT and stromal fibrosis and induced tumor cell death, which was accompanied by the accumulation of M1-macrophages and production of tumor necrosis factor α (TNFα). The CD73-TGFβ dual-blockade promoted a multifaceted inflammatory tumor microenvironment, as shown by the diminished levels of myeloid-derived suppressor cells (MDSCs) and M2-macrophages, and substantially increased levels of activated dendritic cells, cytotoxic T cells, and B cells. Collectively, our results have highlighted a novel strategy for TNBC treatment.
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