Fig. 6From: Interleukin-32θ inhibits tumor-promoting effects of macrophage-secreted CCL18 in breast cancerSchematic diagram of the signaling cascade inhibited by IL-32θ in breast cancer cells. In brief, THP-1-derived macrophages secrete pro-inflammatory factors such as CCL18 to stimulate PKCδ signaling, which can elevate the levels of epithelial-mesenchymal transition (EMT) invasion and migration in breast cancer cells. IL-32θ suppresses these factors by directly interacting with PKCδ to subsequently reduce NF-κB and STAT3 levelsBack to article page