ArticleMolecular cancer2016
CCL18 from ascites promotes ovarian cancer cell migration through proline-rich tyrosine kinase 2 signaling.
Article in Molecular cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 86 citations in OpenAlex.
- Harnessing ovarian cancer ascites for translational science: models, biomarkers, and therapeutics.Molecular cancer · 2025Review
- Defining the Ovarian Cancer Precancerous Landscape through Modeling Fallopian Tube Epithelium Reprogramming Driven by Extracellular Vesicles.Cancer research communications · 2025Article
- Role of tumor microenvironment in ovarian cancer metastasis and clinical advancements.Journal of translational medicine · 2025Review
- PYK2 promotes cell proliferation and epithelial-mesenchymal transition in endometriosis by phosphorylating Snail1.Molecular medicine (Cambridge, Mass.) · 2025Article
- Macrophage diversity in cancer dissemination and metastasis.Cellular & molecular immunology · 2024Review
- From monocyte-derived macrophages to resident macrophages-how metabolism leads their way in cancer.Molecular oncology · 2024Review
- Therapy-induced secretion of spliceosomal components mediates pro-survival crosstalk between ovarian cancer cells.Nature communications · 2024Article
- Histone modification-linked prognostic model for ovarian cancer reveals LBX2 as a novel growth promoter.Journal of cellular and molecular medicine · 2024Article
- Crosstalk of Immune Cells and Platelets in an Ovarian Cancer Microenvironment and Their Prognostic Significance.International journal of molecular sciences · 2023Review
- Revisiting macrophages in ovarian cancer microenvironment: development, function and interaction.Medical oncology (Northwood, London, England) · 2023Review
- Article
- Targeting tumor-associated macrophages for successful immunotherapy of ovarian carcinoma.Journal for immunotherapy of cancer · 2023Review
- Analysis of scRNA-seq and bulk RNA-seq demonstrates the effects of EVI2B or CD361 on CD8Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Activated PyK2 and Its Associated Molecules Transduce Cellular Signaling from the Cancerous Milieu for Cancer Metastasis.International journal of molecular sciences · 2022Review
- Multifaceted role of chemokines in solid tumors: From biology to therapy.Seminars in cancer biology · 2022Review
- CCL18 Expression Is Higher in a Glioblastoma Multiforme Tumor than in the Peritumoral Area and Causes the Migration of Tumor Cells Sensitized by Hypoxia.International journal of molecular sciences · 2022Article
- Spheroid Formation and Peritoneal Metastasis in Ovarian Cancer: The Role of Stromal and Immune Components.International journal of molecular sciences · 2022Review
- A multi-cellular molecular signaling and functional network map of C-C motif chemokine ligand 18 (CCL18): a chemokine with immunosuppressive and pro-tumor functions.Journal of cell communication and signaling · 2022Article
- Chemokine (C-C motif) ligand 18/membrane-associated 3/forkhead box O1 axis promotes the proliferation, migration, and invasion of intrahepatic cholangiocarcinoma.Bioengineered · 2022Article
- Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundOvarian cancer (OC) ascites consist in a proinflammatory tumor environment that is characterized by the presence of various cytokines, chemokines and growth factors. The presence of these inflammatory-related factors in ascites is associated with a more aggressive tumor phenotype. CCL18 is a member of CCL chemokines and its expression has been associated with poor prognosis in some cancers. However, its role in OC progression has not been established. Therefore, the aim of the current study was to elucidate the role of ascites CCL18 in OC progression.
methodsELISA and tissue microarrays were used to assess CCL18 in ascites and phospho-Pyk2 expression in cancer tissues respectively. Cell migration was assessed using Boyden chambers. CCL18 and ascites signaling was examined in ovarian cancer cells utilizing siRNA and exogenous gene expression.
resultsHere, we show that CCL18 levels are markedly increased in advanced serous OC ascites relative to peritoneal effusions from women with benign conditions. Ascites and CCL18 dose-dependently enhanced the migration of OC cell lines CaOV3 and OVCAR3. CCL18 levels in ascites positively correlated with the ability of ascites to promote cell migration. CCL18 blocking antibodies significantly attenuated ascites-induced cell migration. Ascites and CCL18 stimulated the phosphorylation of proline-rich tyrosine kinase 2 (Pyk2) in CaOV3 and OVCAR3 cells. Most importantly, the expression of phosphorylated Pyk2 in serous OC tumors was associated with shorter progression-free survival. Furthermore, enforced expression of Pyk2 promoted tumor cell migration while siRNA-mediated downregulation of Pyk2 attenuated cell migration. Downregulation of Pyk2 markedly inhibited ascites and CCL18-induced cell migration.
conclusionsTaken together, our findings establish an important role for CCL18, as a component of ascites, in the migration of tumor cells and identify Pyk2 as prognostic factor and a critical downstream signaling pathway for ascites-induced OC cell migration.
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