摘要
氧化应激是由活性氧产生和解毒不平衡所致,在决定细胞命运的过程中起着关键的作用。对过量的ros的反应,凋亡信号通路被激活促进正常细胞死亡。然而,通过对生物分子的放松管制,大量的ROS促进了信号因子缺陷的细胞的癌变。在这一行中,nrf 2似乎是m。Aster调节剂,保护细胞免受氧化和亲电应激。nrf 2是一种细胞内转录因子,调节多个基因的表达,编码抗氧化。酶、解毒因子、抗凋亡蛋白和药物转运蛋白。在正常情况下,nrf 2通过与keap 1抑制剂的相互作用而在细胞质中降解,作为泛曲的适配器。氮素然而,大量的ROS激活酪氨酸激酶解离Nrf 2:Keap 1复合物,核导入Nrf 2,协同激活细胞保护基因的表达。永不由于突变和激活的上游致癌基因导致NRF2和/或KAP1的放松、放松与核积累和NRF2的组成性激活有关,以保护细胞免于细胞凋亡。ND诱导细胞增殖、转移和耐药。由于ros和nrf 2信号通路与癌变之间的相互作用,nrf 2的调控似乎在ros和nrf 2的个性化中起着重要的作用。癌症治疗。
关键词: 抗氧化剂,癌症,Keap 1,Nrf 2,ROS,氧化应激。
图形摘要
Current Cancer Drug Targets
Title:Oxidative Stress and Cancer: The Role of Nrf2
Volume: 18 Issue: 6
关键词: 抗氧化剂,癌症,Keap 1,Nrf 2,ROS,氧化应激。
摘要: Oxidative stress due to imbalance between ROS production and detoxification plays a pivotal role in determining cell fate. In response to the excessive ROS, apoptotic signaling pathway is activated to promote normal cell death. However, through deregulation of biomolecules, high amount of ROS promotes carcinogenesis in cells with defective signaling factors. In this line, NRF2 appears to be as a master regulator, which protects cells from oxidative and electrophilic stress. Nrf2 is an intracellular transcription factor that regulates the expression of a number of genes to encode anti-oxidative enzymes, detoxifying factors, anti-apoptotic proteins and drug transporters. Under normal condition, Nrf2 is commonly degraded in cytoplasm by interaction with Keap1 inhibitor as an adaptor for ubiquitination factors. However, high amount of ROS activates tyrosine kinases to dissociate Nrf2: Keap1 complex, nuclear import of Nrf2 and coordinated activation of cytoprotective gene expression. Nevertheless, deregulation of Nrf2 and/or Keap1 due to mutation and activated upstream oncogenes is associated with nuclear accumulation and constitutive activation of Nrf2 to protect cells from apoptosis and induce proliferation, metastasis and chemoresistance. Owning to the interplay of ROS and Nrf2 signaling pathways with carcinogenesis, Nrf2 modulation seems to be important in the personalization of cancer therapy.
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Cite this article as:
Oxidative Stress and Cancer: The Role of Nrf2, Current Cancer Drug Targets 2018; 18 (6) . https://dx.doi.org/10.2174/1568009617666171002144228
DOI https://dx.doi.org/10.2174/1568009617666171002144228 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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