ArticleFrontiers in pharmacology2019
Activation of CXCL6/CXCR1/2 Axis Promotes the Growth and Metastasis of Osteosarcoma Cells
Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Moderate Aerobic Training Causes Muscle Wasting in a DMBA-Induced Sarcoma Rat Model.International journal of molecular sciences · 2026Article
- An integrated single-cell lung cancer atlas reveals distinct fibroblast phenotypes between adenocarcinoma and squamous cell carcinomas.NPJ precision oncology · 2026Article
- Epithelial-Mesenchymal Transition in Osteosarcoma as a Key Driver of Pulmonary Metastasis.Cancers · 2025Review
- Human myocardial-derived highly proliferative cells improve cardiac remodeling after myocardial infarction in mice.The Journal of pharmacology and experimental therapeutics · 2025Article
- Human milk feeding practices and serum immune profiles of one-year-old infants in the CHILD birth cohort study.The American journal of clinical nutrition · 2025Observational
- Chemokines: humble yet mighty players in the tumour microenvironment.Frontiers in immunology · 2025Review
- Transcriptomic analysis reveals TME-mediated macrophage IFIT1 upregulation and CX3CR1 suppression drive osteosarcoma progression.Frontiers in oncology · 2025Article
- Development and experimental verification of novel angiogenesis related prognostic model and immune infiltration characterization in osteosarcoma.Discover oncology · 2024Article
- Review
- CXCL6-CXCR2 axis-mediated PD-L2Heliyon · 2024Article
- Directing B7-H3 chimeric antigen receptor T cell homing through IL-8 induces potent antitumor activity against pediatric sarcoma.Journal for immunotherapy of cancer · 2024Article
- CXCL6: A potential therapeutic target for inflammation and cancer.Clinical and experimental medicine · 2023Review
- Tumor-Associated Macrophages Affect the Tumor Microenvironment and Radioresistance via the Upregulation of CXCL6/CXCR2 in Hepatocellular Carcinoma.Biomedicines · 2023Article
- CXCR2 expression during melanoma tumorigenesis controls transcriptional programs that facilitate tumor growth.Molecular cancer · 2023Article
- Chemokines and cytokines: Axis and allies in prostate cancer pathogenesis.Seminars in cancer biology · 2022Review
- Sulfur mustard single-dose exposure triggers senescence in primary human dermal fibroblasts.Archives of toxicology · 2022Article
- A novel stemness-hypoxia-related signature for prognostic stratification and immunotherapy response in hepatocellular carcinoma.BMC cancer · 2022Article
- Inflammatory and Proliferative Pathway Activation in Human Esophageal Myofibroblasts Treated with Acidic Bile Salts.International journal of molecular sciences · 2022Article
- Extracellular Vesicles Secreted by Corneal Myofibroblasts Promote Corneal Epithelial Cell Migration.International journal of molecular sciences · 2022Article
- Neutrophils: Musketeers against immunotherapy.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma (OS) is a malignant primary bone tumor with high metastatic rate. C-X-C motif chemokine ligand 6 (CXCL6) and its receptor C-X-C motif chemokine receptor 1/2 (CXCR1/2) have been found to participate in the process of carcinogenesis. In this study, we evaluated the role of CXCL6/CXCR1/2 axis in proliferation and metastasis of OS cells. According to our results, the mRNA and protein expressions of CXCL6, CXCR1, and CXCR2 in multiple OS cell lines were determined. Treatment with exogenous CXCL6 for more than 72 h significantly promoted the proliferation of OS cells. Blocking the effect of endogenous CXCL6 restrained the migration, invasion and epithelial-mesenchymal transition (EMT) as evidenced by increased E-cadherin level, decreased N-cadherin and Snail levels in OS cells. On the contrary, exogenous CXCL6 administration enhanced the migration and invasive abilities of OS cells. Moreover, silencing of CXCR1/2 suppressed migration, invasion and EMT of OS cells with or without treatment with exogenous CXCL6. In addition, exogenous CXCL6 promoted the activation of PI3K/AKT and β-catenin signaling pathways, which could be repressed by CXCR2 knockdown. Inactivation of PI3K/AKT or β-catenin pathway by specific inhibitors effectively suppressed CXCL6-induced migration, invasion and EMT of OS cells. Finally, overexpression of CXCL6 significantly contributed to tumor growth, pulmonary metastasis and activation of PI3K/AKT and β-catenin pathways in nude mice
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