Abstract
The liver executes versatile functions and is the chief organ for metabolism of toxicants/xenobiotics. Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and the third foremost cause of cancer death worldwide. Oxidative stress is a key factor related with the development and progression of HCC. Nuclear factor erythroid 2 [NF-E2]-related factor 2 (Nrf2) is a cytosolic transcription factor, which regulates redox homeostasis by activating the expression of an array of antioxidant response element-dependent genes. Nrf2 displays conflicting roles in normal, healthy liver and HCC; in the former, Nrf2 offers beneficial effects, whereas in the latter it causes detrimental effects favouring the proliferation and survival of HCC. Sustained Nrf2 activation has been observed in HCC and facilitates its progression and aggressiveness. This review summarizes the role and mechanism(s) of action of Nrf2 dysregulation in HCC and therapeutic options that can be employed to modulate this transcription factor.
Highlights
Hepatocellular carcinoma (HCC) is the one of the leading liver cancers in many countries and is the fifth most common cancer worldwide [1]
nuclear factor E2-related factor 2 (Nrf2) is the primary player in HCC, as evidenced from the many studies demonstrating an increased expression of Nrf2 associated with HCC
This dysregulated Nrf2 signalling promotes cellular proliferation, triggers vascularization, invasiveness and confers resistance against drugs. This master regulator could serve as a promising therapeutic target in HCC
Summary
Hepatocellular carcinoma (HCC) is the one of the leading liver cancers in many countries and is the fifth most common cancer worldwide [1]. Though liver cirrhosis contributes to 80–90% of HCC development, other factors, viz aflatoxin B1, diabetes, dietary habits, excessive alcohol intake, infection with Hepatitis-B-virus (HBV) and Hepatitis-C-virus (HCV), iron accumulation, non-alcoholic fatty liver disease and tobacco use result in HCC development [2]. Many of these factors modulate the redox homeostasis in the liver, eventually causing hepatocarcinogenesis [3]. Cancers 2018, 10, 481 briefly summarizes the molecular structure, role and potential regulation of Nrf and elaborates upon potential pharmacological strategies that can be used to target this transcription and potential regulation of Nrf and elaborates upon potential pharmacological strategies that factor in cancer. Can be used to target this transcription factor in cancer
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