Recent studies by us demonstrated that GCM is highly effective against alcoholic liver disease, nonalcoholic fatty liver disease, acetaminophen-induced hepatotoxicity, and liver cancer through mechanisms involved in activation of Nrf2 antioxidant system, stimulation of AMPK-mediated energy homeostasis, induction of autophagy degradation process, and inhibiting oncogenic kinase T-lymphokine-activated killer cell-originated protein kinase activity.
Benzyl sulforaphane was superior to SFN in inhibiting Akt/MAPK and activating Nrf2/ARE signalling pathways in HepG2 cells, which indicated that BSFN could be a safe therapeutic strategy for the prevention and treatment of liver cancer.
To understand the mechanism of hepatotoxicity, an attempt has been made to elucidate the role of Nrf2, a transcription factor induced by oxidative stress, in INH induced apoptosis liver cancer cell lines.
This review summarizes the recent understanding of the involvement of Nrf2 in the chemoresistance of liver cancer, its target proteins, expression regulation and potential Nrf2 inhibitors that sensitize chemotherapy drugs in HCC.
Together, these results indicate that MC-LR-induced upregulation of Nrf2 in cancer cells promotes liver cancer cell growth and suggest a positive role of Nrf2 in tumorigenesis.
Together, these results indicate that MC-LR-induced upregulation of Nrf2 in cancer cells promotes liver cancer cell growth and suggest a positive role of Nrf2 in tumorigenesis.