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Figure 3. Major effector pathways of K-RAS and potential interactors. Mutations in K-RAS genes lead to constitutive GTP bound K-RAS proteins that activate downstream phosphorylation cascades. Major effector pathways dysregulated in K-RAS mut cancers are the MAPK (RAF/MEK/ERK) and the PI3K/AKT pathway. Transcription factors regulated by these pathways, as well as STAT3, can bind to the PD-L1 gene, enhancing the transcription rate. TPP destabilizes PD-L1 mRNA at AREs on the 3’UTR region and can be inhibited via MEK signaling in K-RAS mut cancers, prolonging the PD-L1 mRNA’s half-life. This figure was partly created using SMART Servier Medical Art. ARE: AU-rich elements; CR: cytokine receptor; RTK: receptor tyrosine kinase; TTP: tristetraprolin