ArticleNature communications2019
Apoptotic tumor cell-derived microRNA-375 uses CD36 to alter the tumor-associated macrophage phenotype.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 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
93 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.
- Tumor Immune Microenvironment and Its Related miRNAs in Tumor Progression.Frontiers in immunology · 2021Pooled it
- Integrated roles of miR-125b, miR-375, and miR-451 in breast cancer chemoresistance: mechanistic insights and translational implications.Molecular biology reports · 2026Review
- CD36 as a Context-Dependent Regulator of Metabolic Switching in Acute and Chronic Hypoxia.Biomolecules · 2026Review
- CD36 and Its Role in Obesity.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Review
- Mechanoresponsive reprogramming of tumor-associated macrophages during cancer progression.Frontiers in cell and developmental biology · 2026Review
- Targeting the Tumor Immune Microenvironment in Triple-Negative Breast Cancer: The Promise of Polyphenols.Cancers · 2025Review
- Tensins in Cancer: Integration of Their Domain Functions, Context-Dependent Regulation and Biomarker Potential.Biology · 2025Review
- Immune evasion in cancer: mechanisms and cutting-edge therapeutic approaches.Signal transduction and targeted therapy · 2025Review
- Review
- Analyzing the potential targets and mechanism of per- and polyfluoroalkyl substances (PFAS) on breast cancer by integrating network toxicology, single-cell sequencing, spatial transcriptomics, and molecular simulation.Functional & integrative genomics · 2025Article
- Identification of IL-34 and Slc7al as potential key regulators in MASLD progression through epigenomic profiling.Epigenomics · 2025Article
- Adaptive Significance of Non-coding RNAs: Insights from Cancer Biology.Molecular biology and evolution · 2025Review
- Exploring microRNA targeting as a promising approach for solid tumor treatment.Frontiers in oncology · 2025Review
- Chemokine ligand 2: beyond chemotaxis-a multifaceted role in tumor progression.Frontiers in immunology · 2025Review
- Assessing CD36 and CD47 expression levels in solid tumor indications to stratify patients for VT1021 treatment.NPJ precision oncology · 2024Article
- Detailed role of SR-A1 and SR-E3 in tumor biology, progression, and therapy.Cell biochemistry and biophysics · 2024Review
- Biological Roles and Clinical Applications of Exosomes in Breast Cancer: A Brief Review.International journal of molecular sciences · 2024Review
- Development of a First-in-Class RIPK1 Degrader to Enhance Antitumor Immunity.Research square · 2024Article
- Mutual regulation of PD-L1 immunosuppression between tumor-associated macrophages and tumor cells: a critical role for exosomes.Cell communication and signaling : CCS · 2024Review
- Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-immune cell interactions shape the immune cell phenotype, with microRNAs (miRs) being crucial components of this crosstalk. How they are transferred and how they affect their target landscape, especially in tumor-associated macrophages (TAMs), is largely unknown. Here we report that breast cancer cells have a high constitutive expression of miR-375, which is released as a non-exosome entity during apoptosis. Deep sequencing of the miRome pointed to enhanced accumulation of miR-375 in TAMs, facilitated by the uptake of tumor-derived miR-375 via CD36. In macrophages, miR-375 directly targets TNS3 and PXN to enhance macrophage migration and infiltration into tumor spheroids and in tumors of a xenograft mouse model. In tumor cells, miR-375 regulates CCL2 expression to increase recruitment of macrophages. Our study provides evidence for miR transfer from tumor cells to TAMs and identifies miR-375 as a crucial regulator of phagocyte infiltration and the subsequent development of a tumor-promoting microenvironment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.