ArticleFrontiers in immunology2022
SNAI1-dependent upregulation of CD73 increases extracellular adenosine release to mediate immune suppression in TNBC.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Epithelial-mesenchymal transition and immunosuppression: Two sides of the same coin.Cellular and molecular life sciences : CMLS · 2026Review
- Fibronectin Is a Likely Therapeutic Target Shared by Oral and Breast Carcinomas.International journal of molecular sciences · 2026Article
- Near Infrared Photoimmunotherapy for Lung Cancer: Recent Development and Perspective.ImmunoTargets and therapy · 2026Review
- TMB as a predictive biomarker for ICI response in TNBC: current evidence and future directions for augmented anti-tumor responses.Clinical and experimental medicine · 2025Review
- Epithelial-mesenchymal transition orchestrates tumor microenvironment: current perceptions and challenges.Journal of translational medicine · 2025Review
- 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
- Toxoplasma gondii ROP18 induces maternal-fetal dysfunction by downregulating CD73 expression on decidual macrophages.Parasites & vectors · 2025Article
- CD73: a new immune checkpoint for leukemia treatment.Frontiers in immunology · 2025Review
- Epithelial-mesenchymal plasticity in cancer: signaling pathways and therapeutic targets.MedComm · 2024Review
- GRHL2 suppression of NT5E/CD73 in breast cancer cells modulates CD73-mediated adenosine production and T cell recruitment.iScience · 2024Article
- Breaking Barriers: The Promise and Challenges of Immune Checkpoint Inhibitors in Triple-Negative Breast Cancer.Biomedicines · 2024Review
- IGJ suppresses breast cancer growth and metastasis by inhibiting EMT via the NF‑κB signaling pathway.International journal of oncology · 2023Article
- Immune Checkpoint Blockade Therapy for Breast Cancer: Lessons from Epithelial-Mesenchymal Transition.Molecular diagnosis & therapy · 2023Article
- Tumor intrinsic and extrinsic functions of CD73 and the adenosine pathway in lung cancer.Frontiers in immunology · 2023Review
- CD73 regulates zoledronate-induced lymphocyte infiltration in triple-negative breast cancer tumors and lung metastases.Frontiers in immunology · 2023Article
- A role for EMT in CD73 regulation in breast cancer.Oncoimmunology · 2022Article
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative subtype of breast cancer (TNBC) is hallmarked by frequent disease relapse and shows highest mortality rate. Although PD-1/PD-L1 immune checkpoint blockades have recently shown promising clinical benefits, the overall response rate remains largely insufficient. Hence, alternative therapeutic approaches are warranted. Given the immunosuppressive properties of CD73-mediated adenosine release, CD73 blocking approaches are emerging as attractive strategies in cancer immunotherapy. Understanding the precise mechanism regulating the expression of CD73 is required to develop effective anti-CD73-based therapy. Our previous observations demonstrate that the transcription factors driving epithelial-to-mesenchymal transition (EMT-TF) can regulate the expression of several inhibitory immune checkpoints. Here we analyzed the role of the EMT-TF SNAI1 in the regulation of CD73 in TNBC cells. We found that doxycycline-driven SNAI1 expression in the epithelial -like TNBC cell line MDA-MB-468 results in CD73 upregulation by direct binding to the CD73 proximal promoter. SNAI1-dependent upregulation of CD73 leads to increased production and release of extracellular adenosine by TNBC cells and contributes to the enhancement of TNBC immunosuppressive properties. Our data are validated in TNBC samples by showing a positive correlation between the mRNA expression of CD73 and SNAI1. Overall, our results reveal a new CD73 regulation mechanism in TNBC that participates in TNBC-mediated immunosuppression and paves the way for developing new treatment opportunities for CD73-positive TNBC.
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