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. Author manuscript; available in PMC: 2023 Aug 1.
Published in final edited form as: Free Radic Biol Med. 2022 Jun 9;188:146–161. doi: 10.1016/j.freeradbiomed.2022.06.004

Figure 5.

Figure 5.

The antiapoptotic effect of GPx1 upregulation promotes cell survival in some cancers. ASK-1 is maintained in an inactive state by its association with the redox-sensitive thioredoxin (Trx). TNFα-induced oxidative stress can promote the oxidation of thioredoxin, leading to the association of TRAF2 and ASK1 oligomers. These active complexes promote JNK-mediated pathways of apoptosis. In some cancer cells, the presence of GPx1 can decrease the oxidation of Trx to keep ASK-1 in an inactive state. Furthermore, association of GPx1 with TRAF2 may prevent the formation of active ASK1/TRAF2 complexes to block JNK activation and apoptosis. Other mechanisms may promote cells survival in other types of cancer, as discussed in the text.