Li Danjie, Hong Xiaoling, Zhao Feijie, Ci Xinxin, Zhang Songling
Department of Obstetrics and Gynecology, The First Hospital of Jilin University, Changchun, China.
Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Cancer Cell Int. 2021 Feb 17;21(1):116. doi: 10.1186/s12935-021-01822-1.
Acquired resistance to therapeutic drugs has become an important issue in treating ovarian cancer. Studies have shown that the prevalent chemotherapy resistance (cisplatin, paclitaxel etc.) for ovarian cancer occurs partly because of decreased production of reactive oxygen species within the mitochondria of ovarian cancer cells.
Nuclear erythroid-related factor-2 (Nrf2) mainly controls the regulation of transcription of genes through the Keap1-Nrf2-ARE signaling pathway and protects cells by fighting oxidative stress and defending against harmful substances. This protective effect is reflected in the promotion of tumor cell growth and their resistance to chemotherapy drugs. Therefore, inhibition of the Nrf2 pathway may reverse drug resistance. In this review, we describe the functions of Nrf2 in drug resistance based on Nrf2-associated signaling pathways determined in previous studies.
Further studies on the relevant mechanisms of Nrf2 may help improve the outcomes of ovarian cancer therapy.
获得性耐药已成为卵巢癌治疗中的一个重要问题。研究表明，卵巢癌常见的化疗耐药（顺铂、紫杉醇等）部分是由于卵巢癌细胞线粒体内活性氧生成减少所致。
核红细胞相关因子2（Nrf2）主要通过Keap1-Nrf2-ARE信号通路控制基因转录调控，并通过对抗氧化应激和抵御有害物质来保护细胞。这种保护作用体现在促进肿瘤细胞生长及其对化疗药物的耐药性上。因此，抑制Nrf2通路可能会逆转耐药性。在本综述中，我们基于先前研究确定的Nrf2相关信号通路描述了Nrf2在耐药中的作用。
对Nrf2相关机制的进一步研究可能有助于改善卵巢癌治疗效果。
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