Therapeutic potential of chemokine signal inhibition for metastatic breast cancer

Graphical abstract Tumor-infiltrang immune cells such as metastasis-associated macrophages (MAM), regulatory T (Tregreg) cells, and myeloid-derived suppressor cells (MDSC) are reported to promote establishment of the lethal metasta-c foci and restrict efficacy of cytotoxic drugs or tumoricidal immune responses by natural killer (NK) and CD8+ T cells. Recent studies suggest that these pro-tumor immune cells are accumulated a chemokine network established in the tumor microenvironment. Therefore, blockade of these chemokine signals could improve therapeu-c efficacy of chemotherapy and immunotherapy.
Metastatic breast cancer is incurable by current therapies including chemotherapy and immunotherapy. Accumulating evidence indicates that tumor-infiltrating macrophages promote establishment of the lethal metastatic foci and contribute to therapeutic resistance. Recent studies suggest that the accumulation of these macrophages is regulated by a chemokine network established in the tumor microenvironment. In this perspective paper, we elaborate on the chemokine signals that can attract monocytes/macrophages to the site of metastasis, and discuss whether inhibition of these chemokine signals can represent a new therapeutic strategy for metastatic breast cancer.