ArticleCellular oncology (Dordrecht, Netherlands)2021
Epithelial-stromal communication via CXCL1-CXCR2 interaction stimulates growth of ovarian cancer cells through p38 activation.
Article in Cellular oncology (Dordrecht, Netherlands), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026Review
- Identification and evaluation of glutamine-related gene characteristics based on multi-omics to predict the prognosis of patients with colorectal cancer.Journal of translational medicine · 2026Article
- Candidate Biomarkers for Crohn's Disease: Hub Genes and Regulatory miRNAs Identified by Bioinformatics Analysis.Biochemistry research international · 2026Article
- Potential of CXCR1/2 as a target for the treatment of inflammation and cancer (Review).Experimental and therapeutic medicine · 2025Review
- Direct Targeting of CXCR2 Receptor Inhibits Neuroblastoma Growth: An In Vitro Assessment.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Association between cytokines and progression-free survival in ovarian cancer following CRS/HIPEC treatment.Journal of ovarian research · 2025Article
- OCT4 promotes lung cancer progression through upregulation of VEGF-correlated chemokine-1.International journal of medical sciences · 2025Article
- Targeting IL-8 and Its Receptors in Prostate Cancer: Inflammation, Stress Response, and Treatment Resistance.Cancers · 2024Review
- CCL28 promotes progression of hepatocellular carcinoma through PDGFD-regulated MMP9 and VEGFA pathways.Discover oncology · 2024Article
- Enhancing precision medicine: a nomogram for predicting platinum resistance in epithelial ovarian cancer.World journal of surgical oncology · 2024Article
- The role of CXCL family members in different diseases.Cell death discovery · 2023Review
- CXCR2 expression during melanoma tumorigenesis controls transcriptional programs that facilitate tumor growth.Molecular cancer · 2023Article
- Involvement in Tumorigenesis and Clinical Significance of CXCL1 in Reproductive Cancers: Breast Cancer, Cervical Cancer, Endometrial Cancer, Ovarian Cancer and Prostate Cancer.International journal of molecular sciences · 2023Review
- Tumor-secreted exosomal miR-141 activates tumor-stroma interactions and controls premetastatic niche formation in ovarian cancer metastasis.Molecular cancer · 2023Article
- Prognostic Significance of the CXCLs and Its Impact on the Immune Microenvironment in Ovarian Cancer.Disease markers · 2023Article
- Comprehensive bioinformatic analysis constructs a CXCL model for predicting survival and immunotherapy effectiveness in ovarian cancer.Frontiers in pharmacology · 2023Article
- The Role of CXC Chemokines in Cancer Progression.Cancers · 2022Review
- Potential Pro-Tumorigenic Effect of Bisphenol A in Breast Cancer via Altering the Tumor Microenvironment.Cancers · 2022Review
- Alpha-Linolenic Acid Modulates T Cell Incorporation in a 3D Tissue-Engineered Psoriatic Skin Model.Cells · 2022Article
- Extracellular Vesicles Secreted by Corneal Myofibroblasts Promote Corneal Epithelial Cell Migration.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeParacrine interactions with the stromal environment, including fibroblasts, may be important in the pathogenesis of ovarian cancer. Here, we evaluated the effect of conditioned media derived from ovarian fibroblasts (fibroblast-CMs) and their major cytokines on the growth of ovarian cancer cells, as well as the involvement of mitogen-activated protein kinases (MAPKs) and AKT in mediating this effect.
methodsOvarian cancer cells were cultured in serum-free media (SF), or conditioned media of fibroblasts derived from normal ovary (CM1) and ovarian tumor tissue (CM2). Cell proliferation was measured by MTT assay. Phosphorylation of MAPKs and AKT was evaluated by Western blotting. Specific inhibitors of MAPKs and AKT were used to evaluate their respective involvement in mediating increased cell growth. Cytokine levels in fibroblast-CMs were measured using Luminex assays. Immunohistochemical staining was conducted for CXCL1, CXCR2 and phosphorylated p38 in primary ovarian tumors.
resultsCM1 and CM2 significantly increased the growth of ovarian cancer cells relative to SF. In OVCAR3 and OVCAR4 cells, p38 phosphorylation was strongly induced by fibroblast-CMs, and pre-treatment with a p38 inhibitor prevented the growth increase induced by fibroblast-CMs. Fibroblasts secreted high levels of IL-6, IL-8, MCP1 and CXCL1. Treatment with only CXCL1 (1 μg/ml) increased cell growth and p38 phosphorylation. Treatment with a CXCR2 inhibitor effectively prevented p38 activation and cell growth induced by fibroblast-CMs. High expression of both CXCL1 and CXCR2 correlated with high expression of phosphorylated p38 in primary ovarian tumors.
conclusionsFrom our data, we conclude that CXCL1 is a key factor derived from ovarian fibroblasts that is responsible for increased ovarian cancer cell growth in part through p38 activation. Phosphorylated p38 can be used as a biomarker to predict CXCL1-CXCR2 interaction in vivo.
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