Fig. 1
From: ROS and TGFβ: from pancreatic tumour growth to metastasis
The crosstalk between TGFβ ligand activation, ROS levels and the canonical and non-canonical TGFβ pathways. ROS can activate latent TGFβ ligand in extracellular matrix but also stimulate the expression and secretion of TGFβ, and mediate the effects of TGFβ by modulating the activities of both canonical Smads pathway and non-canonical pathways: Ras-Raf-MEK-ERK, TAK1-JNK/p38, TRAFs-NFκB, and PI3K-AKT. In turn, TGFβ can directly stimulate ROS production through mitochondria and Noxs. TGFβ can also increase ROS levels through the canonical Smad2/3/4 pathway and non-canonical MEK/ERK pathway by suppressing the expression of several antioxidant enzymes or stimulating the expression of NOXs genes. Direct (solid arrows) or indirect (dash arrows) activation, and indirection inhibition (dash inhibitor) are shown