Fig. 4.

Signaling pathway related with cancer development. PRDX1 enhances the transactivation potential of NF-κB in ER-deficient breast cancer cells and upregulates phosphorylation of NF-κB subunit in bladder cancers. PRDX1 promotes tumorigenesis of esophageal squamous cell carcinoma through regulating the activity of mTOR/p70S6K pathway. PRDX2 is involved in the regulation of Wnt/β-catenin signaling in colorectal cancer cells. Specifically, PRDX2 inhibits GSK-3β activity, enhances β-catenin translocation into the nucleus, and inhibits the levels of β-catenin phosphorylation, thus resulting in significant up-regulation of transcription of the LEF/TCF target genes c-Myc and Survivin. PRDX3 is associated with NF-κB signaling pathway. PRDX3 enhances I-κB phosphorylation and induces NF-κB signaling pathway. PRDX3 also acts synergistically with MAP3K13 to regulate the activation of NF-κB in the cytosol. PRDX4 binds with Srx and the Srx-PRDX4 axis contributes to the maintenance of lung tumor phenotype by AP-1 and MAPK signaling pathway. PRDX6 promotes tumor development via the JAK2/STAT3 pathway in a urethane-induced lung tumor model. Upregulation of PRDX6 results in the activation of Akt via PI3K and p38 kinase.