ArticleOncotarget2016
Targeted gene silencing of CCL2 inhibits triple negative breast cancer progression by blocking cancer stem cell renewal and M2 macrophage recruitment.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
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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
76 citing papers in PubMed, 116 citations in OpenAlex.
- Trial
- Hydrogen suppressed tumor growth during chronic intermittent hypoxia via modulating macrophage polarization.Scientific reports · 2026Article
- Halogenated anthraquinones in breast cancer therapy: Structural modifications targeting VEGF-related angiogenesis pathways.Journal of pharmaceutical analysis · 2026Review
- The chemokine network in triple-negative breast cancer: its role in immune microenvironment regulation, and prospects for targeted therapy.Frontiers in immunology · 2026Review
- The Anticancer Effect of Kaempferol Through Downregulation of CDKs and PD-L1 in Triple-Negative Breast Cancer Cells.Cancers · 2025Article
- Cooperative CCL2/CCR2 and HGF/MET signaling enhances breast cancer growth and invasion associated with metabolic reprogramming.Cancer biology & therapy · 2025Article
- Prospective study of cesarean scar pregnancy associated with increased MCP-1 and cholesterol synthesis.Biomedical reports · 2025Article
- Silibinin Anticancer Effects Through the Modulation of the Tumor Immune Microenvironment in Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Review
- Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition.Journal of hematology & oncology · 2025Review
- Roles of tumor-associated macrophages in triple-negative breast cancer progression.Frontiers in immunology · 2025Review
- Macrophages: Key Players in the Battle against Triple-Negative Breast Cancer.International journal of molecular sciences · 2024Review
- CD8Molecular medicine reports · 2024Article
- CCL2 signaling promotes skeletal muscle wasting in non-tumor and breast tumor models.Disease models & mechanisms · 2024Article
- Tumor associated macrophages as key contributors and targets in current and future therapies for melanoma.Expert review of clinical immunology · 2024Review
- The Anticancer Effects and Therapeutic Potential of Kaempferol in Triple-Negative Breast Cancer.Nutrients · 2024Review
- Bifunctionality and Antitumor Efficacy of ZG-126, a Vitamin D Receptor Agonist/Histone Deacetylase Inhibitor Hybrid Molecule.Journal of medicinal chemistry · 2024Article
- Decoding the Tumour Microenvironment: Molecular Players, Pathways, and Therapeutic Targets in Cancer Treatment.Cancers · 2024Review
- Molecular targets and therapeutic strategies for triple-negative breast cancer.Molecular biology reports · 2023Review
- MCP-1 expression in breast cancer and its association with distant relapse.Cancer medicine · 2023Article
- Hypoxia-induced CCL2/CCR2 axis in adipose-derived stem cells (ADSCs) promotes angiogenesis by human dermal microvascular endothelial cells (HDMECs) in flap tissues.Journal of physiology and biochemistry · 2023Article
16 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
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple negative breast cancers are an aggressive subtype of breast cancer, characterized by the lack of estrogen receptor, progesterone receptor and Her2 expression. Triple negative breast cancers are non-responsive to conventional anti-hormonal and Her2 targeted therapies, making it necessary to identify new molecular targets for therapy. The chemokine CCL2 is overexpressed in invasive breast cancers, and regulates breast cancer progression through multiple mechanisms. With few approaches to target CCL2 activity, its value as a therapeutic target is unclear. In these studies, we developed a novel gene silencing approach that involves complexing siRNAs to TAT cell penetrating peptides (Ca-TAT) through non-covalent calcium cross-linking. Ca-TAT/siRNA complexes penetrated 3D collagen cultures of breast cancer cells and inhibited CCL2 expression more effectively than conventional antibody neutralization. Ca-TAT/siRNA complexes targeting CCL2 were delivered to mice bearing MDA-MB-231 breast tumor xenografts. In vivo CCL2 gene silencing inhibited primary tumor growth and metastasis, associated with a reduction in cancer stem cell renewal and recruitment of M2 macrophages. These studies are the first to demonstrate that targeting CCL2 expression in vivo may be a viable therapeutic approach to treating triple negative breast cancer.
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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.