Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages
The tumor microenvironment is rich in multiple cell types that influence tumor development. Macrophages infiltrate tumors, where they are the most abundant immune cell population and secrete a number of cytokines. Aspirin acts as a chemopreventive agent against cancer development. This study investi...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2018/6380643 |
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| author | Chia-Chien Hsieh Chih-Hsuan Wang |
| author_facet | Chia-Chien Hsieh Chih-Hsuan Wang |
| author_sort | Chia-Chien Hsieh |
| collection | DOAJ |
| description | The tumor microenvironment is rich in multiple cell types that influence tumor development. Macrophages infiltrate tumors, where they are the most abundant immune cell population and secrete a number of cytokines. Aspirin acts as a chemopreventive agent against cancer development. This study investigated whether aspirin regulates crosstalk between breast cancer cells and macrophages. To study these interactions in a tumor microenvironment, a conditioned media was employed using 4T1 breast cancer cells cultured in RAW 264.7 cell-conditioned medium (RAW-CM), and a cocultured model of both cells was used. When 4T1 cells were cultured in the RAW-CM, there were increases in cell viability and secretion of the cytokines VEGF, PAI-1, TNF-α, and IL-6. Treatment with aspirin inhibited 4T1 cell growth and migration and MCP-1, PAI-1, and IL-6 production. In the coculture of both cells, aspirin inhibited secretion of MCP-1, IL-6, and TGF-β. Furthermore, aspirin significantly decreased the M2 macrophage marker CD206, but increased M1 marker CD11c expression. In summary, aspirin treatment inhibited the crosstalk of 4T1 and RAW 264.7 cells through regulation of angiogenic and inflammatory mediator production and influenced the M1/M2 macrophage subtype. This highlighted that aspirin suppresses the tumor favorable microenvironment and could be a promising agent against triple-negative breast cancer. |
| format | Article |
| id | doaj-art-ed9c99f8b5d044928044e89a2fe43238 |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-ed9c99f8b5d044928044e89a2fe432382025-08-20T02:22:10ZengWileyMediators of Inflammation0962-93511466-18612018-01-01201810.1155/2018/63806436380643Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and MacrophagesChia-Chien Hsieh0Chih-Hsuan Wang1Department of Human Development and Family Studies, National Taiwan Normal University, Taipei, TaiwanDepartment of Human Development and Family Studies, National Taiwan Normal University, Taipei, TaiwanThe tumor microenvironment is rich in multiple cell types that influence tumor development. Macrophages infiltrate tumors, where they are the most abundant immune cell population and secrete a number of cytokines. Aspirin acts as a chemopreventive agent against cancer development. This study investigated whether aspirin regulates crosstalk between breast cancer cells and macrophages. To study these interactions in a tumor microenvironment, a conditioned media was employed using 4T1 breast cancer cells cultured in RAW 264.7 cell-conditioned medium (RAW-CM), and a cocultured model of both cells was used. When 4T1 cells were cultured in the RAW-CM, there were increases in cell viability and secretion of the cytokines VEGF, PAI-1, TNF-α, and IL-6. Treatment with aspirin inhibited 4T1 cell growth and migration and MCP-1, PAI-1, and IL-6 production. In the coculture of both cells, aspirin inhibited secretion of MCP-1, IL-6, and TGF-β. Furthermore, aspirin significantly decreased the M2 macrophage marker CD206, but increased M1 marker CD11c expression. In summary, aspirin treatment inhibited the crosstalk of 4T1 and RAW 264.7 cells through regulation of angiogenic and inflammatory mediator production and influenced the M1/M2 macrophage subtype. This highlighted that aspirin suppresses the tumor favorable microenvironment and could be a promising agent against triple-negative breast cancer.http://dx.doi.org/10.1155/2018/6380643 |
| spellingShingle | Chia-Chien Hsieh Chih-Hsuan Wang Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages Mediators of Inflammation |
| title | Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages |
| title_full | Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages |
| title_fullStr | Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages |
| title_full_unstemmed | Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages |
| title_short | Aspirin Disrupts the Crosstalk of Angiogenic and Inflammatory Cytokines between 4T1 Breast Cancer Cells and Macrophages |
| title_sort | aspirin disrupts the crosstalk of angiogenic and inflammatory cytokines between 4t1 breast cancer cells and macrophages |
| url | http://dx.doi.org/10.1155/2018/6380643 |
| work_keys_str_mv | AT chiachienhsieh aspirindisruptsthecrosstalkofangiogenicandinflammatorycytokinesbetween4t1breastcancercellsandmacrophages AT chihhsuanwang aspirindisruptsthecrosstalkofangiogenicandinflammatorycytokinesbetween4t1breastcancercellsandmacrophages |