ArticleOncotarget2016
CCL5 promotes VEGF-C production and induces lymphangiogenesis by suppressing miR-507 in human chondrosarcoma 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 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Uncovering host transcriptional responses to tilapia lake virus (TiLV) through De novo RNA-seq assembly in Nile tilapia, Oreochromis niloticus.Archives of virology · 2026Article
- Macrophages recruited by implanted fibrin gels promote regeneration of injured lymphatic vessels.Scientific reports · 2026Article
- CCR-CCL axes as key upstream influencers of pancreatic ductal adenocarcinoma: CCR2-CCL2, CCR5-CCL5, CCR4-CCL17/22, CCR6-CCL20, CCR7-CCL19/21.Frontiers in immunology · 2026Review
- Pipelines for lymphocyte homeostasis maintenance during cancer immunotherapy.Frontiers in immunology · 2025Review
- PITX1 as a grading, prognostic and tumor-infiltrating immune cells marker for chondrosarcoma: a public database-based immunoassay and tissue sample analysis.Frontiers in oncology · 2025Article
- Visfatin Facilitates VEGF-D-Induced Lymphangiogenesis through Activating HIF-1α and Suppressing miR-2277-3p in Human Chondrosarcoma.International journal of molecular sciences · 2024Article
- The Landscape of microRNAs in Bone Tumor: A Comprehensive Review in Recent Studies.MicroRNA (Shariqah, United Arab Emirates) · 2024Review
- Review
- Review
- Assessment of the RANTES Level Correlation and Selected Inflammatory and Pro-Angiogenic Molecules Evaluation of Their Influence on CRC Clinical Features: A Preliminary Observational Study.Medicina (Kaunas, Lithuania) · 2022Observational
- The lymphatic vasculature: An active and dynamic player in cancer progression.Medicinal research reviews · 2022Review
- Identification of medicinal compounds as potential inhibitors for mutated isocitrate dehydrogenases against chondrosarcoma.Saudi journal of biological sciences · 2022Article
- Leronlimab, a humanized monoclonal antibody to CCR5, blocks breast cancer cellular metastasis and enhances cell death induced by DNA damaging chemotherapy.Breast cancer research : BCR · 2021Article
- c-Myc promotes lymphatic metastasis of pancreatic neuroendocrine tumor through VEGFC upregulation.Cancer science · 2021Article
- Review
- CC Chemokines in a Tumor: A Review of Pro-Cancer and Anti-Cancer Properties of Receptors CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10 Ligands.International journal of molecular sciences · 2020Review
- Hypoxia Alters the Expression of CC Chemokines and CC Chemokine Receptors in a Tumor-A Literature Review.International journal of molecular sciences · 2020Review
- The CCL5/CCR5 Axis in Cancer Progression.Cancers · 2020Review
- The G protein coupled receptor CCR5 in cancer.Advances in cancer research · 2020Review
- Recent Advances Targeting CCR5 for Cancer and Its Role in Immuno-Oncology.Cancer research · 2019Review
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chondrosarcoma is the second most frequently occurring type of bone malignancy that is characterized by the distant metastasis propensity. Vascular endothelial growth factor-C (VEGF-C) is the major lymphangiogenic factor, and makes crucial contributions to tumor lymphangiogenesis and lymphatic metastasis. Chemokine CCL5 has been reported to facilitate angiogenesis and metastasis in chondrosarcoma. However, the effect of chemokine CCL5 on VEGF-C regulation and lymphangiogenesis in chondrosarcoma has largely remained a mystery. In this study, we showed a clinical correlation between CCL5 and VEGF-C as well as tumor stage in human chondrosarcoma tissues. We further demonstrated that CCL5 promoted VEGF-C expression and secretion in human chondrosarcoma cells. The conditioned medium (CM) from CCL5-overexpressed cells significantly induced tube formation of human lymphatic endothelial cells (LECs). Mechanistic investigations showed that CCL5 activated VEGF-C-dependent lymphangiogenesis by down-regulating miR-507. Moreover, inhibiting CCL5 dramatically reduced VEGF-C and lymphangiogenesis in the chondrosarcoma xenograft animal model. Collectively, we document for the first time that CCL5 induces tumor lymphangiogenesis by the induction of VEGF-C in human cancer cells. Our present study reveals miR-507/VEGF-C signaling as a novel mechanism in CCL5-mediated tumor lymphangiogenesis. Targeting both CCL5 and VEGF-C pathways might serve as the potential therapeutic strategy to block cancer progression and metastasis in chondrosarcoma.
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