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NRF2 activation induced by PML-RARα promotes microRNA 125b-1 expression and confers resistance to chemotherapy in acute promyelocytic leukemia.

作者信息

Yu Xibao, Mansouri Ardalan, Liu Zhuandi, Gao Rili, Li Kehan, Chen Cunte, Huang Youxue, Chen Zheng, Chen Shaohua, Lu Yuhong, Li Yangqiu, Zeng Chengwu, Zeng Yixin

机构信息

Department of Experimental Research, Sun Yat-Sen University Cancer Center, State Key Laboratory Oncology in South China, Guangzhou, China.

Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China.

出版信息

Clin Transl Med. 2021 May;11(5):e418. doi: 10.1002/ctm2.418.

DOI:10.1002/ctm2.418
PMID:34047481
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8101532/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3677/8101532/b35a955a24f0/CTM2-11-e418-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3677/8101532/6e7fae4b6442/CTM2-11-e418-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3677/8101532/80c1a67066a2/CTM2-11-e418-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3677/8101532/cbafbbcdcbd2/CTM2-11-e418-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3677/8101532/b35a955a24f0/CTM2-11-e418-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3677/8101532/6e7fae4b6442/CTM2-11-e418-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3677/8101532/80c1a67066a2/CTM2-11-e418-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3677/8101532/cbafbbcdcbd2/CTM2-11-e418-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3677/8101532/b35a955a24f0/CTM2-11-e418-g002.jpg

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1
NRF2 activation induced by PML-RARα promotes microRNA 125b-1 expression and confers resistance to chemotherapy in acute promyelocytic leukemia.由早幼粒细胞白血病锌指蛋白-维甲酸受体α（PML-RARα）诱导的核因子E2相关因子2（NRF2）激活可促进微小RNA 125b-1的表达，并赋予急性早幼粒细胞白血病对化疗的抗性。
Clin Transl Med. 2021 May;11(5):e418. doi: 10.1002/ctm2.418.
2
Leukemic cellular retinoic acid resistance and missense mutations in the PML-RARalpha fusion gene after relapse of acute promyelocytic leukemia from treatment with all-trans retinoic acid and intensive chemotherapy.急性早幼粒细胞白血病经全反式维甲酸和强化化疗治疗后复发，出现白血病细胞维甲酸耐药及PML-RARα融合基因错义突变。
Blood. 1998 Aug 15;92(4):1172-83.
3
Acute promyelocytic leukemia: a novel PML/RARalpha fusion that generates a frameshift in the RARalpha transcript and ATRA resistance.急性早幼粒细胞白血病：一种新型的PML/RARα融合基因，该融合基因导致维甲酸受体α（RARα）转录本发生移码突变并产生全反式维甲酸（ATRA）耐药。
Leuk Lymphoma. 2007 Mar;48(3):489-96. doi: 10.1080/10428190601136163.
4
Novel mutation in the PML/RARalpha chimeric gene exhibits dramatically decreased ligand-binding activity and confers acquired resistance to retinoic acid in acute promyelocytic leukemia.PML/RARα嵌合基因中的新型突变表现出显著降低的配体结合活性，并赋予急性早幼粒细胞白血病对维甲酸的获得性耐药。
Exp Hematol. 2001 Jul;29(7):864-72. doi: 10.1016/s0301-472x(01)00651-8.
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Mutations in the E-domain of RAR portion of the PML/RAR chimeric gene may confer clinical resistance to all-trans retinoic acid in acute promyelocytic leukemia.PML/RAR嵌合基因RAR部分的E结构域突变可能致使急性早幼粒细胞白血病对全反式维甲酸产生临床耐药性。
Blood. 1998 Jul 15;92(2):374-82.
6
MicroRNA-125b Accelerates and Promotes PML-RARa-driven Murine Acute Promyelocytic Leukemia.微小 RNA-125b 促进并加速 PML-RARa 驱动的小鼠急性早幼粒细胞白血病。
Biomed Environ Sci. 2022 Jun 20;35(6):485-493. doi: 10.3967/bes2022.067.
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Targeting of PML/RARalpha is lethal to retinoic acid-resistant promyelocytic leukemia cells.靶向PML/RARα对维甲酸耐药的早幼粒细胞白血病细胞具有致死性。
Blood. 1998 Sep 1;92(5):1758-67.
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The PML-RARalpha fusion protein and targeted therapy for acute promyelocytic leukemia.早幼粒细胞白血病的PML-RARα融合蛋白与靶向治疗
Leuk Lymphoma. 2004 Apr;45(4):639-48. doi: 10.1080/10428190310001609933.
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Altered ligand binding and transcriptional regulation by mutations in the PML/RARalpha ligand-binding domain arising in retinoic acid-resistant patients with acute promyelocytic leukemia.在急性早幼粒细胞白血病的维甲酸耐药患者中，因PML/RARα配体结合域突变导致配体结合和转录调控改变。
Blood. 2000 Nov 1;96(9):3200-8.
10
Reduced retinoic acid-sensitivities of nuclear receptor corepressor binding to PML- and PLZF-RARalpha underlie molecular pathogenesis and treatment of acute promyelocytic leukemia.核受体共抑制因子与早幼粒细胞白血病（PML）及早幼粒细胞白血病锌指蛋白（PLZF）-维甲酸受体α（RARα）结合时视黄酸敏感性降低是急性早幼粒细胞白血病分子发病机制及治疗的基础。
Blood. 1998 Apr 15;91(8):2634-42.

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Inhibition of NRF2 enhances the acute myeloid leukemia cell death induced by venetoclax via the ferroptosis pathway.抑制NRF2可通过铁死亡途径增强维奈托克诱导的急性髓系白血病细胞死亡。
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Targeting NRF2 uncovered an intrinsic susceptibility of acute myeloid leukemia cells to ferroptosis.

本文引用的文献

1
Arsenic Trioxide Rescues Structural p53 Mutations through a Cryptic Allosteric Site.三氧化二砷通过隐秘变构位点挽救结构 p53 突变。
Cancer Cell. 2021 Feb 8;39(2):225-239.e8. doi: 10.1016/j.ccell.2020.11.013. Epub 2020 Dec 24.
2
PML/RARa Interferes with NRF2 Transcriptional Activity Increasing the Sensitivity to Ascorbate of Acute Promyelocytic Leukemia Cells.PML/RARα干扰NRF2转录活性，增加急性早幼粒细胞白血病细胞对维生素C的敏感性。
Cancers (Basel). 2019 Dec 30;12(1):95. doi: 10.3390/cancers12010095.
3
Controversy about pharmacological modulation of Nrf2 for cancer therapy.
靶向NRF2揭示了急性髓系白血病细胞对铁死亡的内在易感性。
Exp Hematol Oncol. 2023 May 17;12(1):47. doi: 10.1186/s40164-023-00411-4.
4
High expression of LOC541471, GDAP1, SOD1, and STK25 is associated with poor overall survival of patients with acute myeloid leukemia.LOC541471、GDAP1、SOD1 和 STK25 的高表达与急性髓系白血病患者的总体生存不良相关。
Cancer Med. 2023 Apr;12(7):9055-9067. doi: 10.1002/cam4.5644. Epub 2023 Jan 27.
5
Disulfiram, an aldehyde dehydrogenase inhibitor, works as a potent drug against sepsis and cancer via NETosis, pyroptosis, apoptosis, ferroptosis, and cuproptosis.双硫仑是一种乙醛脱氢酶抑制剂，通过中性粒细胞胞外陷阱形成、细胞焦亡、细胞凋亡、铁死亡和铜死亡，作为一种有效的抗败血症和抗癌药物发挥作用。
Blood Sci. 2022 Jul 1;4(3):152-154. doi: 10.1097/BS9.0000000000000117. eCollection 2022 Jul.
6
BET bromodomain inhibition rescues PD-1-mediated T-cell exhaustion in acute myeloid leukemia.BET 溴结构域抑制挽救了 PD-1 介导的急性髓系白血病中的 T 细胞耗竭。
Cell Death Dis. 2022 Aug 2;13(8):671. doi: 10.1038/s41419-022-05123-x.
7
STAT6/VDR Axis Mitigates Lung Inflammatory Injury by Promoting Nrf2 Signaling Pathway.STAT6/VDR 轴通过促进 Nrf2 信号通路减轻肺炎症性损伤。
Oxid Med Cell Longev. 2022 Jan 10;2022:2485250. doi: 10.1155/2022/2485250. eCollection 2022.
关于Nrf2的药物调节用于癌症治疗的争议。
Redox Biol. 2017 Aug;12:727-732. doi: 10.1016/j.redox.2017.04.013. Epub 2017 Apr 8.
4
NRF2-driven miR-125B1 and miR-29B1 transcriptional regulation controls a novel anti-apoptotic miRNA regulatory network for AML survival.NRF2驱动的miR-125B1和miR-29B1转录调控控制了一个用于急性髓系白血病存活的新型抗凋亡微小RNA调控网络。
Cell Death Differ. 2015 Apr;22(4):654-64. doi: 10.1038/cdd.2014.152. Epub 2014 Oct 17.
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MIR125B1 represses the degradation of the PML-RARA oncoprotein by an autophagy-lysosomal pathway in acute promyelocytic leukemia.MIR125B1通过自噬-溶酶体途径抑制急性早幼粒细胞白血病中PML-RARA癌蛋白的降解。
Autophagy. 2014 Oct 1;10(10):1726-37. doi: 10.4161/auto.29592. Epub 2014 Jul 18.
6
Trafficking of the transcription factor Nrf2 to promyelocytic leukemia-nuclear bodies: implications for degradation of NRF2 in the nucleus.转录因子 Nrf2 向早幼粒细胞白血病核体的转运：对核内 NRF2 降解的影响。
J Biol Chem. 2013 May 17;288(20):14569-14583. doi: 10.1074/jbc.M112.437392. Epub 2013 Mar 29.
7
The high Nrf2 expression in human acute myeloid leukemia is driven by NF-κB and underlies its chemo-resistance.人急性髓系白血病中 Nrf2 的高表达受 NF-κB 驱动，是其化疗耐药的基础。
Blood. 2012 Dec 20;120(26):5188-98. doi: 10.1182/blood-2012-04-422121. Epub 2012 Oct 17.
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Camptothecin induces apoptosis in cancer cells via microRNA-125b-mediated mitochondrial pathways.喜树碱通过 microRNA-125b 介导的线粒体途径诱导癌细胞凋亡。
Mol Pharmacol. 2012 Apr;81(4):578-86. doi: 10.1124/mol.111.076794. Epub 2012 Jan 17.
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Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis.癌基因诱导的 Nrf2 转录促进 ROS 解毒和肿瘤发生。
Nature. 2011 Jul 6;475(7354):106-9. doi: 10.1038/nature10189.
10
PML/RARalpha targets promoter regions containing PU.1 consensus and RARE half sites in acute promyelocytic leukemia.PML/RARalpha 靶定急性早幼粒细胞白血病中含有 PU.1 共有序列和 RARE 半位点的启动子区域。
Cancer Cell. 2010 Feb 17;17(2):186-97. doi: 10.1016/j.ccr.2009.12.045.