Targeting Nrf2 may reverse the drug resistance in ovarian cancer

BackgroundAcquired resistance to therapeutic drugs has become an important issue in treating ovarian cancer. Studies have shown that the prevalent chemotherapy resistance (cisplatin, paclitaxel etc.) for ovarian cancer occurs partly because of decreased production of reactive oxygen species within the mitochondria of ovarian cancer cells.Main BodyNuclear erythroid-related factor-2 (Nrf2) mainly controls the regulation of transcription of genes through the Keap1-Nrf2-ARE signaling pathway and protects cells by fighting oxidative stress and defending against harmful substances. This protective effect is reflected in the promotion of tumor cell growth and their resistance to chemotherapy drugs. Therefore, inhibition of the Nrf2 pathway may reverse drug resistance. In this review, we describe the functions of Nrf2 in drug resistance based on Nrf2-associated signaling pathways determined in previous studies.ConclusionsFurther studies on the relevant mechanisms of Nrf2 may help improve the outcomes of ovarian cancer therapy.

Automated summary

Nrf2 plays a crucial role in regulating gene transcription through the Keap1-Nrf2-ARE signaling pathway, protecting cells from oxidative stress and harmful substances. Inhibiting the Nrf2 pathway may reverse drug resistance in ovarian cancer cells.