Fig. 7.
Schematic model illustatrating the redox regulation of PD-L1 expression through growth factor signaling. Activation of K-rasG12V promotes ROS generation due to K-ras-induced mitochondrial dysfunction. The elevated ROS promotes FGFR1 expression at the transcriptional level. The signals from growth factor receptors (FGFR1 and EGFR) activate the Akt signaling pathway, which enhances the transcription of PD-L1 gene, leading to a significant increase of PD-L1 mRNA and protein. The subsequent interaction of PD-L1 with PD-1 on T cells lead to immunosuppression.