ArticleOncotarget2016
CCL3 promotes angiogenesis by dysregulation of miR-374b/ VEGF-A axis in human osteosarcoma cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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.
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Who cites it
61 citing papers in PubMed, 91 citations in OpenAlex.
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- Synergistic TCR-independent action of IL-33 and IL-12 drive a potent IFNγ secretory program in human circulating MAIT cells with immunomodulatory properties.Frontiers in immunology · 2026Article
- Article
- Single-cell transcriptome analysis reveals abnormal angiogenesis and placentation by loss of imprinted glutaminyl-peptide cyclotransferase.Journal of Zhejiang University. Science. B · 2025Article
- Boosting tumor homing of endogenous natural killer cells via therapeutic secretomes of chemically primed natural killer cells.Journal for immunotherapy of cancer · 2025Article
- Transcriptomic analysis reveals TME-mediated macrophage IFIT1 upregulation and CX3CR1 suppression drive osteosarcoma progression.Frontiers in oncology · 2025Article
- Developing a 3D bone model of osteosarcoma to investigate cancer mechanisms and evaluate treatments.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- miR-374 family is a key regulator of chronic primary pain onset.Pain reports · 2024Article
- Targeting PADI2 as a potential therapeutic strategy against metastasis in oral cancer via suppressing EMT-mediated migration and invasion and CCL3/5-induced angiogenesis.Clinical & experimental metastasis · 2024Article
- Identifying microRNAs Possibly Implicated in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Fibromyalgia: A Review.International journal of molecular sciences · 2024Review
- Macrophage Inflammatory Proteins (MIPs) Contribute to Malignant Potential of Colorectal Polyps and Modulate Likelihood of Cancerization Associated with Standard Risk Factors.International journal of molecular sciences · 2024Article
- Targeting the chemokines in acute graft-versus-host disease.Frontiers in immunology · 2024Review
- Hypoxia-regulated exosomes mediate M2 macrophage polarization and promote metastasis in chondrosarcoma.Aging · 2023Article
- Promise and Challenges of T Cell Immunotherapy for Osteosarcoma.International journal of molecular sciences · 2023Review
- The Role of CCL3 in the Pathogenesis of Rheumatoid Arthritis.Rheumatology and therapy · 2023Review
- Comprehensive analysis of angiogenesis pattern and related immune landscape for individual treatment in osteosarcoma.NPJ precision oncology · 2023Article
- Current Trends in Vascular Biomarkers for Systemic Sclerosis: A Narrative Review.International journal of molecular sciences · 2023Review
- Genetically predicted circulating levels of cytokines and the risk of oral cavity and pharyngeal cancer: a bidirectional mendelian-randomization study.Frontiers in genetics · 2023Article
- Potential Anti-Metastatic Role of the Novel miR-CT3 in Tumor Angiogenesis and Osteosarcoma Invasion.International journal of molecular sciences · 2022Article
- An overview of resistance to chemotherapy in osteosarcoma and future perspectives.Cancer drug resistance (Alhambra, Calif.) · 2022Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma is the most frequent bone tumor, characterized by a high metastatic potential. However, the crosstalk between chemokine (C-C motif) ligand 3 (CCL3), which facilitates tumor progression and metastasis. Vascular endothelial growth factor-A (VEGF-A), an angiogenesis inducer and a highly specific mitogen for endothelial cells, has not been well explored in human osteosarcoma. Here we demonstrate the correlation of CCL3 and VEGF-A expressions, quantified by immunohistochemistry, with the tumor stage of human osteosarcoma tissues. Furthermore, CCL3 promotes VEGF-A expression in human osteosarcoma cells that subsequently induces human endothelial progenitor cell (EPC) migration and tube formation. Phosphorylation of JNK, ERK, and p38 was found after CCL3 stimulation. In addition, JNK, ERK, and p38 inhibitors also abolished CCL3-induced VEGF-A expression and angiogenesis. We noted that CCL3 reduces the expression of miR-374b and miR-374b mimic by reversing CCL3-promoted VEGF-A expression and angiogenesis in vitro and in vivo. This study shows that CCL3 promotes VEGF-A expression and angiogenesis in human osteosarcoma cells by down-regulating miR-374b expression via JNK, ERK, and p38 signaling pathways. Thus, CCL3 may be a new molecular therapeutic target in osteosarcoma angiogenesis and metastasis.
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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.