CSF-1R in Cancer: More than a Myeloid Cell Receptor

CSF-1R in Cancer: More than a Myeloid Cell Receptor

9 January 2024 | Francesca Cersosimo, Silvia Lonardi, Cristina Ulivieri, Paolo Martini, Andrea Morrione, William Vermi, Antonio Giordano and Emanuele Giurisato
The review discusses the role of the colony-stimulating factor 1 receptor (CSF-1R) in cancer beyond its traditional function as a myeloid cell receptor. CSF-1R is a tyrosine kinase receptor primarily expressed on monocytes and macrophages, playing a key role in immune responses and cell differentiation. However, recent studies have shown that CSF-1R is also expressed on cancer cells, where it contributes to tumor progression by promoting cell proliferation, migration, stemness, and chemoresistance. CSF-1R signaling can be autocrine, with cancer cells producing its ligands, leading to enhanced tumor growth. The receptor is involved in the development of an immunosuppressive tumor microenvironment and the recruitment of tumor-associated macrophages (TAMs). CSF-1R expression is associated with poor prognosis in various cancers, including breast, ovarian, and colorectal cancers. The receptor's expression is regulated by multiple factors, including oncogenic mutations and signaling pathways such as TGF-β and MEK/ERK. Therapeutic strategies targeting CSF-1R, including monoclonal antibodies and small-molecule inhibitors, are being explored to block its pro-oncogenic effects. The review highlights the importance of understanding CSF-1R expression and function in cancer cells, as well as the potential for developing targeted therapies. While much is known about CSF-1R in myeloid cells, its role in cancer cells remains an area of active research, with implications for improving cancer treatment outcomes.The review discusses the role of the colony-stimulating factor 1 receptor (CSF-1R) in cancer beyond its traditional function as a myeloid cell receptor. CSF-1R is a tyrosine kinase receptor primarily expressed on monocytes and macrophages, playing a key role in immune responses and cell differentiation. However, recent studies have shown that CSF-1R is also expressed on cancer cells, where it contributes to tumor progression by promoting cell proliferation, migration, stemness, and chemoresistance. CSF-1R signaling can be autocrine, with cancer cells producing its ligands, leading to enhanced tumor growth. The receptor is involved in the development of an immunosuppressive tumor microenvironment and the recruitment of tumor-associated macrophages (TAMs). CSF-1R expression is associated with poor prognosis in various cancers, including breast, ovarian, and colorectal cancers. The receptor's expression is regulated by multiple factors, including oncogenic mutations and signaling pathways such as TGF-β and MEK/ERK. Therapeutic strategies targeting CSF-1R, including monoclonal antibodies and small-molecule inhibitors, are being explored to block its pro-oncogenic effects. The review highlights the importance of understanding CSF-1R expression and function in cancer cells, as well as the potential for developing targeted therapies. While much is known about CSF-1R in myeloid cells, its role in cancer cells remains an area of active research, with implications for improving cancer treatment outcomes.
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