Fig. 3

Activation and function of NOX4 in epithelial-mesenchymal transition (EMT). Mechanism by which NOX4-dependent ROS production is activated by TGF-β1 signaling and its contribution to the regulation of EMT. NOX4 expression is upregulated by TGF-β1 through the activation pathway SMAD or NF-κB, which enhances H₂O₂ production. NOX4 can produce O₂⁻ using 10% of the electron flow, which is rapidly converted to H₂O₂ with the help of SOD, or it can directly generate H₂O₂ using the remaining 90% of the electron flow. The figure shows how these ROS affect key EMT markers by modulating signaling pathways such as the PI3K/AKT/HIF-1α axis, increasing the expression of mesenchymal markers like Vimentin and N-cadherin, while decreasing the epithelial marker E-cadherin, thereby enhancing cancer cell invasiveness