Autophagy, an evolutionarily conserved catabolic process, is the most important pathogenic events in the development and progression of liver diseases. Deregulation of Nrf2 is proposed to play a key pathogenic role in hepatocellular carcinoma (HCC). Under certain pathophysiological conditions, such as oxidative stress, impaired autophagy is accompanied by the Nrf2 activation that leads to the detrimental effects favoring the proliferation and survival of HCC. Elucidating its role and potential mechanism is essential for understanding tumorigenesis and the development of effective clinical application. Nrf2 is participated in HCC proliferation, migration and invasion through autophagy pathways. These includes the negatively regulated-Nrf2 by Keap1 that participates in HCC tumorigenesis via regulating ROS production, in which autophagy may contribute to oxidant metabolic reprogramming of HCC cells. Post-transcriptional modifications, such as phosphorylation and ubiquitination of Nrf2, can be positively or negatively induced by multiple transcription factors. Nrf2 exhibits chemoresistance through its binding sites in the promoter region of the target genes. Nrf2 may be a valuable potential biomarker and therapeutic strategy for diagnostics, prognostics and treatment of HCC.

中文翻译：

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自噬诱导的肝细胞癌中的核因子红系2（NF-E2）相关因子2（Nrf2）。

自噬是进化上保守的分解代谢过程，是肝病发展和进程中最重要的致病事件。Nrf2的失调被提议在肝细胞癌（HCC）中起关键的致病作用。在某些病理生理条件下，例如氧化应激，自噬功能受损会伴随Nrf2活化，从而导致不利于HCC增殖和存活的有害作用。阐明其作用和潜在机制对于理解肿瘤发生和有效临床应用的发展至关重要。Nrf2通过自噬途径参与HCC的增殖，迁移和侵袭。其中包括Keap1负调控的Nrf2，它通过调节ROS的产生参与HCC的肿瘤发生，其中自噬可能有助于HCC细胞的氧化剂代谢重编程。转录后修饰，例如Nrf2的磷酸化和泛素化，可以被多种转录因子阳性或阴性诱导。Nrf2通过其在靶基因启动子区域的结合位点表现出化学抗性。Nrf2可能是用于HCC诊断，预后和治疗的有价值的潜在生物标志物和治疗策略。