Fig. 3
From: ROS and TGFβ: from pancreatic tumour growth to metastasis
Combined targeting of ROS and TGFβ as cancer therapy. Canonical and non-canonical TGFβ signalling inhibitors could be combined with ROS induction to increase the effectiveness of therapeutic strategies for cancer. These mechanisms would impact fibrosis, immunity regulation, extracellular matrix (ECM) deposition, as well as cancer stem cell (CSC) self-renewal and epithelial-mesenchymal transition, tumour metastasis and angiogenesis. Combinational targeting of TGFβ activators, instead of targeting TGFβ alone, may further increase efficiency and specificity of treatment. Positive regulations (arrows) and negative regulations (inhibitors) are shown in the figure. MMP: matrix metalloproteinases; DC: dendritic cell; NK: natural killer cell; M1: classically-activated macrophage; M2: wound-healing macrophage (also known as alternatively-activated macrophage; Th1: type 1 T helper cell; Th2: type 2 T helper cell; Treg: and regulatory T cells