ArticleFrontiers in immunology2015
Crosstalk between Tumor Cells and Macrophages in Stroma Renders Tumor Cells as the Primary Source of MCP-1/CCL2 in Lewis Lung Carcinoma.
Article in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- The prognostic significance of CCL2 in oral squamous cell carcinoma: insights from tissue expression and perioperative serum profiling.Frontiers in oncology · 2026Article
- The CCL2-CCR2 axis in primary lung cancer and pulmonary metastasis: from molecular mechanisms to therapeutic potentials.Frontiers in immunology · 2026Review
- Bcl6 drives stem-like memory macrophages differentiation to foster tumor progression.Cellular and molecular life sciences : CMLS · 2022Article
- Identification of the JNK-Active Triple-Negative Breast Cancer Cluster Associated With an Immunosuppressive Tumor Microenvironment.Journal of the National Cancer Institute · 2022Article
- Roles of Interleukin-1 Receptor Antagonist in Prostate Cancer Progression.Biomedicines · 2020Article
- Article
- Positive Allosteric Modulation of CD11b as a Novel Therapeutic Strategy Against Lung Cancer.Frontiers in oncology · 2020Article
- Emerging role of mTOR in tumor immune contexture: Impact on chemokine-related immune cells migration.Theranostics · 2020Review
- Cancer Cell-Derived Granulocyte-Macrophage Colony-Stimulating Factor Is Dispensable for the Progression of 4T1 Murine Breast Cancer.International journal of molecular sciences · 2019Article
- Inflammation induced by incomplete radiofrequency ablation accelerates tumor progression and hinders PD-1 immunotherapy.Nature communications · 2019Article
- More Than Just Attractive: How CCL2 Influences Myeloid Cell Behavior Beyond Chemotaxis.Frontiers in immunology · 2019Review
- High levels of CCL2 or CCL4 in the tumor microenvironment predict unfavorable survival in lung adenocarcinoma.Thoracic cancer · 2018Article
- The chemokine MCP-1 (CCL2) in the host interaction with cancer: a foe or ally?Cellular & molecular immunology · 2018Review
- Targeting Macrophage-Recruiting Chemokines as a Novel Therapeutic Strategy to Prevent the Progression of Solid Tumors.Frontiers in immunology · 2018Review
- Effect of TALEN-mediated IL-6 knockout on cell proliferation, apoptosis, invasion and anti-cancer therapy in hepatocellular carcinoma (HCC-LM3) cells.Oncotarget · 2017Article
- Dusp3 deletion in mice promotes experimental lung tumour metastasis in a macrophage dependent manner.PloS one · 2017Article
- CCL2/EGF positive feedback loop between cancer cells and macrophages promotes cell migration and invasion in head and neck squamous cell carcinoma.Oncotarget · 2016Article
- CCN: core regulatory proteins in the microenvironment that affect the metastasis of hepatocellular carcinoma?Oncotarget · 2016Review
- Induction of Monocyte Chemoattractant Proteins in Macrophages via the Production of Granulocyte/Macrophage Colony-Stimulating Factor by Breast Cancer Cells.Frontiers in immunology · 2016Article
- Cilia in autophagy and cancer.Cilia · 2015Review
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
The chemokine MCP-1/CCL2 is produced by a variety of tumors and plays an important role in cancer progression. We and others previously demonstrated that the primary source of MCP-1 in several mouse tumors, including 4T1 breast cancer, M5076 sarcoma, and B16 melanoma, was stromal cells. In the present study, we identified that tumor cells were the primary source of MCP-1 in Lewis lung carcinoma (LLC), because MCP-1 mRNA was highly expressed in tumors grown in both wild type (WT) and MCP-1(-/-) mice with elevated serum MCP-1 levels. Since LLC cells isolated from tumors expressed low levels of MCP-1 in vitro, it appeared that the tumor-stromal cell interaction in a tumor microenvironment increased MCP-1 expression in LLC cells. In fact, co-culture of LLC cells with normal mouse peritoneal macrophages or normal lung cells containing macrophages increased MCP-1 expression by LLC cells. Macrophages from TNFα(-/-) mice failed to activate LLC cells and anti-TNFα neutralizing antibody abolished the effect of WT macrophages on LLC cells. When LLC cells were transplanted into TNFα(-/-) mice, the levels of MCP-1 mRNA in tumors and serum MCP-1 levels were markedly lower as compared to WT mice, and importantly, tumors grew more slowly. Taken together, our results indicate that TNFα released by tumor cell-activated macrophages is critical for increased MCP-1 production by tumors cells. Thus, disruption of tumor-stromal cell interaction may inhibit tumor progression by reducing the production of tumor-promoting proinflammatory mediators, such as MCP-1.
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