Stimulatory versus suppressive effects of GM-CSF on tumor progression in multiple cancer types

Granulocyte-macrophage colony-stimulating factor (GM-CSF, also called CSF-2) is best known for its critical role in immune modulation and hematopoiesis. A large body of experimental evidence indicates that GM-CSF, which is frequently upregulated in multiple types of human cancers, effectively marks cancer cells with a ‘danger flag’ for the immune system. In this context, most studies have focused on its function as an immunomodulator, namely its ability to stimulate dendritic cell (DC) maturation and monocyte/macrophage activity. However, recent studies have suggested that GM-CSF also promotes immune-independent tumor progression by supporting tumor microenvironments and stimulating tumor growth and metastasis. Although some studies have suggested that GM-CSF has inhibitory effects on tumor growth and metastasis, an even greater number of studies show that GM-CSF exerts stimulatory effects on tumor progression. In this review, we summarize a number of findings to provide the currently available information regarding the anticancer immune response of GM-CSG. We then discuss the potential roles of GM-CSF in the progression of multiple types of cancer to provide insights into some of the complexities of its clinical applications. Tumor progression: Multiple roles of immune response protein More research is needed to understand the relationship between tumor progression and an immune-response-related protein. In-Sun Hong from South Korea ' s Gachon University, Incheon, reviewed recent research on “ granulocyte-macrophage colony-stimulating factor ” (GM-CSF), a protein that regulates the differentiation of stem cells in the bone marrow into immune cells. Clinical trials have shown that GM-CSF can be used to promote an immune response against some kinds of cancers, such as metastatic melanoma. However, there is growing evidence that cells unrelated to the immune system also produce GM-CSF, sometimes promoting tumor growth, such as in some skin and lung cancers, and at other times inhibiting it, such as in some colorectal cancers. More detailed knowledge of the interactions between GM-CSF and tumors is needed to improve clinical outcomes in the future.