Role of NRF2 in Ovarian Cancer.
Giovanni TossettaSonia FantoneEva MontanariDaniela MarzioniGaia GoteriPublished in: Antioxidants (Basel, Switzerland) (2022)
Among gynaecologic malignancies, ovarian cancer is one of the most dangerous, with a high fatality rate and relapse due to the occurrence of chemoresistance. Many researchers demonstrated that oxidative stress is involved in tumour occurrence, growth and development. Nuclear factor erythroid 2-related factor 2 (NRF2) is an important transcription factor, playing an important role in protecting against oxidative damage. Increased levels of Reactive Oxygen Species (ROS) activate NRF2 signalling, inducing the expression of antioxidant enzymes, such as haem oxygenase (HO-1), catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD), that protect cells against oxidative stress. However, NRF2 activation in cancer cells is responsible for the development of chemoresistance, inactivating drug-mediated oxidative stress that normally leads to cancer cells' death. In this review, we report evidence from the literature describing the effect of NRF2 on ovarian cancer, with a focus on its function in drug resistance, NRF2 natural and synthetic modulators and its protective function in normal ovarian preservation.
Keyphrases
- oxidative stress
- induced apoptosis
- dna damage
- ischemia reperfusion injury
- diabetic rats
- reactive oxygen species
- nuclear factor
- transcription factor
- risk assessment
- poor prognosis
- systematic review
- toll like receptor
- hydrogen peroxide
- emergency department
- cell death
- small molecule
- cell cycle arrest
- heat shock
- nitric oxide
- cell proliferation
- inflammatory response
- free survival
- amyotrophic lateral sclerosis