ArticleClinical & experimental metastasis2020
CCL2 secreted from cancer-associated mesothelial cells promotes peritoneal metastasis of ovarian cancer cells through the P38-MAPK pathway.
Article in Clinical & experimental metastasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 60 citations in OpenAlex.
- Review
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- Reversing chemoresistance in ovarian cancer: network pharmacology reveals how hydroxychloroquine/sulfasalazine duotherapy remodels tumor inflammatory-immune microenvironment.Frontiers in immunology · 2026Article
- Apoptosis of Mesothelial Cells Is Associated with the Pattern of Peritoneal Metastases in Ovarian Cancer.Cancers · 2025Article
- MAPK signaling reprogramming via integrative TCM-Western medicine strategy: mechanistic interactions between bioactive herbal components and chemotherapy in ovarian cancer therapy - a comprehensive review.Journal of ovarian research · 2025Review
- CCL2/CCR2 signaling pathway in tumorigenesis and metastasis (Review).Oncology letters · 2025Review
- NR4A3high mast cells promote ovarian cancer metastasis by reprogramming tumor-associated macrophages via JAK2/STAT6 signaling.Translational oncology · 2025Article
- Role of tumor microenvironment in ovarian cancer metastasis and clinical advancements.Journal of translational medicine · 2025Review
- Chemokine (C-C Motif) Ligand 2/CCR2/Extracellular Signal-Regulated Kinase Signal Induced through Cancer Cell-Macrophage Interaction Contributes to Hepatocellular Carcinoma Progression.The American journal of pathology · 2025Article
- Exploring miRNA profile associated with cisplatin resistance in ovarian cancer cells.Biochemistry and biophysics reports · 2025Article
- The silent spread: exploring diverse metastatic pathways in high-grade serous ovarian cancer.Frontiers in medicine · 2025Review
- Relationship between adipocytes and hematological tumors in the bone marrow microenvironment: a literature review.Translational cancer research · 2024Review
- M2-like tumor-associated macrophage-secreted CCL2 facilitates gallbladder cancer stemness and metastasis.Experimental hematology & oncology · 2024Article
- Hydrophobic surface induced pro-metastatic cancer cells forBioactive materials · 2024Article
- The role and therapeutic targeting of the CCL2/CCR2 signaling axis in inflammatory and fibrotic diseases.Frontiers in immunology · 2024Review
- Cancer-Associated Fibroblast-Induced Remodeling of Tumor Microenvironment in Recurrent Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Cancer-mesothelial and cancer-macrophage interactions in the ovarian cancer microenvironment.American journal of physiology. Cell physiology · 2023Review
- Vascular Dysfunctions Contribute to the Long-Term Cognitive Deficits Following COVID-19.Biology · 2023Review
- Article
- CC Chemokine 2 Promotes Ovarian Cancer Progression through the MEK/ERK/MAP3K19 Signaling Pathway.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial ovarian cancer (EOC) is considered to secrete various factors in order to promote peritoneal dissemination through cell-to-cell interaction between cancer and mesothelial cells. We previously revealed that TGF-β secreted from EOC induces normal human peritoneal mesothelial cells (HPMCs) to differentiate into cancer-associated mesothelial cells (CAMCs). However, the relationship between tumor cells and CAMCs in EOC is still unclear. We hypothesized that CAMCs also secrete chemokines that attract cancer cells and induce peritoneal dissemination of EOC. We examined chemokines secreted from HPMCs and CAMCs by human chemokine array, and revealed that conditioned medium of CAMCs (CAMCs-CM) included many types of chemokines. The signals of CCL2 were the highest compared with other chemokines. The secretion and relative expression of CCL2 were significantly higher in CAMCs. Recombinant CCL2 promoted trans-mesothelial migration of HPMCs and the migration and invasion by EOC cells. In addition, CCL2 secreted from CAMCs promoted invasion of EOC cells. Furthermore, the neutralizing antibody of CCL2 reduced invasion by EOC. Clinical outcomes of patients whose tissue expressed higher CCR2 were significantly poorer than in patients whose tissue expression was lower. CCL2 activated the phosphorylation of p38 mitogen-activated protein kinase (MAPK). In addition, CAMCs-CM activated the p38 MAPK pathway. Phosphorylation of p38 MAPK reduced with the presence of neutralizing antibody of CCL2. In conclusion, these data indicate CCL2 in CAMCs-CM promoted the malignant potential of EOC. CCL2 plays a crucial role in the tumor microenvironment of EOC.
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