| First Author | Sundaram S | Year | 2019 |
| Journal | Anticancer Res | Volume | 39 |
| Issue | 4 | Pages | 1729-1738 |
| PubMed ID | 30952712 | Mgi Jnum | J:290233 |
| Mgi Id | MGI:6442347 | Doi | 10.21873/anticanres.13279 |
| Citation | Sundaram S, et al. (2019) Adipose-specific Monocyte Chemotactic Protein-1 Deficiency Reduces Pulmonary Metastasis of Lewis Lung Carcinoma in Mice. Anticancer Res 39(4):1729-1738 |
| abstractText | AIM: Monocyte chemotactic protein-1 (MCP1) is a potent adipokine. This study tested the hypothesis that adipose-produced MCP1 contributes to metastasis. MATERIALS AND METHODS: In a spontaneous metastasis model of Lewis lung carcinoma (LLC), male adipose MCP1-deficient (Mcp1(-/-)) and wild-type (WT) mice were fed the AIN93G diet or a high-fat diet (HFD) for 11 weeks. Lung metastasis from a subcutaneous tumor was the primary endpoint. RESULTS: The adipose expression of MCP1 was lower in Mcp1(-/-) mice than in WT controls. The HFD increased the number of lung metastases in WT mice. The number of metastasis was significantly lower in the HFD-fed Mcp1(-/-) mice than in the HFD-fed WT mice. Compared to the WT mice, adipose MCP1 deficiency lowered plasma concentrations of insulin, proinflammatory adipokines (leptin, plasminogen activator inhibitor-1, and resistin), and angiogenic markers (vascular endothelial growth factor, hepatocyte growth factor, and angiopoietin-2). CONCLUSION: Adipose MCP1 deficiency attenuates HFD-enhanced pulmonary metastasis of LLC. |
