Macrophage inflammatory factors promote epithelial-mesenchymal transition in breast cancer
PDF | HTML | How to cite
Metrics: PDF 1674 views | HTML 2426 views | ?
Robert B. Bednarczyk1, Neha Y. Tuli1, Elyse K. Hanly1, Ghada Ben Rahoma1, Rachana Maniyar1, Abraham Mittelman1, Jan Geliebter1 and Raj K. Tiwari1
1Department of Microbiology and Immunology, New York Medical College, Valhalla, NY, USA
Raj K. Tiwari, email: [email protected]
Keywords: epithelial-mesenchymal transition; inflammation; M1 macrophages; metastasis; secretory factors
Received: June 03, 2017 Accepted: September 05, 2017 Epub: March 23, 2018 Published: May 11, 2018
The majority of breast cancers (90–95%) arise due to mediators distinct from inherited genetic mutations. One major mediator of breast cancer involves chronic inflammation. M1 macrophages are an integral component of chronic inflammation and the breast cancer tumor microenvironment (TME). Previous studies have demonstrated that up to 50% of the breast tumor comprise of tumor-associated macrophages (TAMs) and increased TAM infiltration has been associated with poor patient prognosis. Furthermore, breast cancer associated deaths are predominantly attributed to invasive cancers and metastasis with epithelial-mesenchymal transition (EMT) being implicated. In this study, we investigated the effects of cellular crosstalk between TAMs and breast cancer using an in vitro model system. M1 polarized THP-1 macrophage conditioned media (CM) was generated and used to evaluate cellular and functional changes of breast cancer lines T47D and MCF-7. We observed that T47D and MCF-7 exhibited a partial EMT phenotype in the presence of activated THP-1 CM. Additionally, MCF-7 displayed a significant increase in migratory and invasive properties. We conclude that M1 secretory factors can promote a partial EMT of epithelial-like breast cancer cells. The targeting of M1 macrophages or their secretory components may inhibit EMT and limit the invasive potential of breast cancer.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.