Abstract
Abstract Breast cancer (BC) is one of the leading causes of cancer-related deaths among women worldwide. Interleukin-12 (IL-12) has demonstrated anti-cancer effects in vitro and in vivo. IL-12 signaling occurs mainly through STAT4, and it induces anti-tumorigenic actions such as promotion of apoptosis, differentiation of T helper 1 (Th1) cells, increasing immune cell’s cytotoxicity and preventing angiogenesis. The role of the IL-12/STAT4 axis in human breast cancer has not been studied thoroughly. Our aim was to assess if the IL-12/STAT4 pathway is differentially expressed and contribute to a pro-tumor environment in BC. We hypothesize that genetic and molecular impairments lead to a downregulation of the IL-12/STAT4 axis and are associated with breast cancer risk. mRNA and protein levels of key IL-12/STAT4 molecules were measured using peripheral mononuclear blood cells (PBMCs) from BC patients and non-BC controls. Interleukin-12 B (IL12B), STAT4 and interferon gamma (IFNG) expression was lower in BC samples when compared with the controls. These results suggest that the IL-12/STAT4 axis pathway is differentially expressed in BC, and prompts more specific analyses such as whether this is BC subtype-specific.
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