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Article(id=1324078554195042389, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1324078333767594037, articleNumber=null, orderNo=null, doi=10.20043/j.cnki.MPM.202507326, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1752768000000, receivedDateStr=2025-07-18, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1793614527509, onlineDateStr=2026-11-02, pubDate=1767974400000, pubDateStr=2026-01-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793614527509, onlineIssueDateStr=2026-11-02, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793614527509, creator=13701087609, updateTime=1793614527509, updator=13701087609, issue=Issue{id=1324078333767594037, tenantId=1146029695717560320, journalId=1227665162245664772, year='2026', volume='53', issue='1', pageStart='1', pageEnd='192', issueExtLink='null', onlineDate='null', pubDate='1767974400000', pubDateStr='2026-01-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1793614474956, creator='13701087609', updateTime=1793614571752, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1324078739914621270, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1324078333767594037, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1324078739914621271, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1324078333767594037, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=188, endPage=192, ext={EN=ArticleExt(id=1324078554425729110, articleId=1324078554195042389, tenantId=1146029695717560320, journalId=1227665162245664772, language=EN, title=Research progress on the mechanisms by which Nrf2 promotes triple-negative breast cancer progression, columnId=1228016569138213037, journalTitle=Modern Preventive Medicine, columnName=Clinical Medicine and Prevention, runingTitle=null, highlight=null, articleAbstract=
Objective

Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype characterized by its propensity for metastasis and poor prognosis, with pathogenesis closely linked to oxidative stress, metabolic reprogramming, and tumor microenvironment. As a key regulator of antioxidant responses, nuclear factor erythroid 2-related factor 2 (Nrf2) promotes TNBC progression by orchestrating antioxidant defense mechanisms, ferroptosis-protective systems, metabolic reprogramming, and remodeling of the tumor microenvironment. This review summarizes current advances in the mechanisms by which Nrf2 drives TNBC progression, with a particular focus on the molecular pathways through which it regulates oxidative stress,metabolic reprogramming, and the tumor microenvironment to promote tumor progression. Additionally, it evaluates the potential applications of Nrf2 in preventive medicine and public health, providing a theoretical foundation for early intervention and targeted therapy in TNBC.

, authors=Hui-min GAN, Jun-qiang SHI, Rui-jiao CHEN, authorsList=Hui-min GAN, Jun-qiang SHI, Rui-jiao CHEN, authorCompany=null, correspAuthors=Rui-jiao CHEN, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1324078554723524695, articleId=1324078554195042389, tenantId=1146029695717560320, journalId=1227665162245664772, language=CN, title=Nrf2促进三阴性乳腺癌进展机制的研究进展, columnId=1228016570119680182, journalTitle=现代预防医学, columnName=临床与预防, runingTitle=null, highlight=null, articleAbstract=
目的

三阴性乳腺癌（triple-negative breast cancer，TNBC）是一种恶性程度高、易转移且预后差的乳腺癌亚型，其发病机制主要与氧化应激、代谢重编码、肿瘤微环境密切相关。Nrf2作为关键的调控因子，通过调控抗氧化防御机制、铁死亡防御系统、代谢重编程、肿瘤微环境促进TNBC进展。本文综述了Nrf2在TNBC进展中的作用机制，重点探讨其通过调控氧化应激、代谢重编码、肿瘤微环境促进肿瘤进展的分子通路，并分析其在预防医学和公共卫生领域的潜在应用价值，为TNBC的早期干预和靶向治疗提供理论依据。

, authors=甘慧敏, 石俊强, 陈瑞蛟, authorsList=甘慧敏, 石俊强, 陈瑞蛟, authorCompany=null, correspAuthors=陈瑞蛟, authorNote=

甘慧敏（1986—），女，硕士，编辑，研究方向：肿瘤及慢性病防治

, correspAuthorsNote=
陈瑞蛟，E-mail:
, copyrightStatement=本刊刊出的所有文章不代表中华预防医学会和本刊编委会的观点，除非特别声明。, copyrightOwner=中华预防医学会和四川大学华西公共卫生学院, extLink=null, articleAbsUrl=null, sourceXml=P4K35uW1r5ejL8hbm8HIKQ==, magXml=WA/XvZkPqDHz75OVoKjICg==, pdfUrl=null, pdf=YKDVv4UyoMHDhuAc+AW4lg==, pdfFileSize=600821, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=lMGDMJebrlc1CTXp9uxxIw==, mapNumber=null, fund=null)}, authors=[Author(id=1324078555172315228, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1324078554195042389, orderNo=0, firstName=null, middleName=null, lastName=null, nameCn=null, orcid=null, stid=null, country=null, authorPic=null, dead=0, email=null, emailSecond=null, emailThird=null, correspondingAuthor=0, authorType=1, ext={EN=AuthorExt(id=1324078555348475998, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1324078554195042389, authorId=1324078555172315228, language=EN, stringName=Hui-min GAN, firstName=Hui-min, middleName=null, lastName=GAN, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=null, address=Jining Medical University, Jining, Shandong 272067, China, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null), CN=AuthorExt(id=1324078555415584863, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1324078554195042389, authorId=1324078555172315228, language=CN, stringName=甘慧敏, firstName=null, middleName=null, lastName=null, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=null, address=济宁医学院，山东 济宁 272067, bio={"content":"

甘慧敏（1986—），女，硕士，编辑，研究方向：肿瘤及慢性病防治

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甘慧敏（1986—），女，硕士，编辑，研究方向：肿瘤及慢性病防治

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Nrf2促进三阴性乳腺癌进展机制的研究进展
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甘慧敏 , 石俊强 , 陈瑞蛟
现代预防医学 | 临床与预防 2026,53(1): 188-192
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现代预防医学 |临床与预防 2026 , 53 (1) : 188 -192
Nrf2促进三阴性乳腺癌进展机制的研究进展
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甘慧敏, 石俊强, 陈瑞蛟
作者信息
  • 济宁医学院，山东 济宁 272067
通讯作者:
陈瑞蛟，E-mail:
作者简介:

甘慧敏（1986—），女，硕士，编辑，研究方向：肿瘤及慢性病防治

Research progress on the mechanisms by which Nrf2 promotes triple-negative breast cancer progression
Hui-min GAN, Jun-qiang SHI, Rui-jiao CHEN
Affiliations
  • Jining Medical University, Jining, Shandong 272067, China
出版时间: 2026-01-10 doi: 10.20043/j.cnki.MPM.202507326
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摘要
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目的

三阴性乳腺癌（triple-negative breast cancer，TNBC）是一种恶性程度高、易转移且预后差的乳腺癌亚型，其发病机制主要与氧化应激、代谢重编码、肿瘤微环境密切相关。Nrf2作为关键的调控因子，通过调控抗氧化防御机制、铁死亡防御系统、代谢重编程、肿瘤微环境促进TNBC进展。本文综述了Nrf2在TNBC进展中的作用机制，重点探讨其通过调控氧化应激、代谢重编码、肿瘤微环境促进肿瘤进展的分子通路，并分析其在预防医学和公共卫生领域的潜在应用价值，为TNBC的早期干预和靶向治疗提供理论依据。

Nrf2  /  三阴性乳腺癌  /  氧化应激  /  代谢重编程  /  肿瘤微环境
Objective

Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype characterized by its propensity for metastasis and poor prognosis, with pathogenesis closely linked to oxidative stress, metabolic reprogramming, and tumor microenvironment. As a key regulator of antioxidant responses, nuclear factor erythroid 2-related factor 2 (Nrf2) promotes TNBC progression by orchestrating antioxidant defense mechanisms, ferroptosis-protective systems, metabolic reprogramming, and remodeling of the tumor microenvironment. This review summarizes current advances in the mechanisms by which Nrf2 drives TNBC progression, with a particular focus on the molecular pathways through which it regulates oxidative stress,metabolic reprogramming, and the tumor microenvironment to promote tumor progression. Additionally, it evaluates the potential applications of Nrf2 in preventive medicine and public health, providing a theoretical foundation for early intervention and targeted therapy in TNBC.

Nrf2  /  Triple-negative breast cancer  /  Oxidative stress  /  Metabolic reprogramming  /  Tumor microenvironment
甘慧敏, 石俊强, 陈瑞蛟. Nrf2促进三阴性乳腺癌进展机制的研究进展. 现代预防医学, 2026 , 53 (1) : 188 -192 . DOI: 10.20043/j.cnki.MPM.202507326
Hui-min GAN, Jun-qiang SHI, Rui-jiao CHEN. Research progress on the mechanisms by which Nrf2 promotes triple-negative breast cancer progression[J]. Modern Preventive Medicine, 2026 , 53 (1) : 188 -192 . DOI: 10.20043/j.cnki.MPM.202507326
正文
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乳腺癌（breast cancer）是女性最常见的恶性肿瘤，据统计，2024年美国女性新发乳腺癌约31万例，占女性恶性肿瘤的首位；2022年中国女性乳腺癌发病人数超35万例，发病率仅次于肺癌[1]。乳腺癌不同分子亚型，其治疗策略与预后迥异。Luminal A型、Luminal B型（HR+/HER2-） 乳腺癌可从内分泌治疗中显著获益；HER-2过表达型则可接受高效的HER-2靶向治疗[2]。而三阴性乳腺癌（triple-negative breast cancer, TNBC）约占所有乳腺癌的10%～20%，因ER、PR及HER-2均为阴性表达，无法从内分泌和靶向治疗中受益。目前化疗仍是其主要的传统治疗手段，但临床效果有限，预后差，临床表现易复发、易转移等特点。患者确诊后五年内生存率不足15%，早期转移和治疗抵抗是导致TNBC临床进展的主要原因。因此，深入阐明影响TNBC进展的分子机制，并寻找有效的干预靶点，已成为乳腺癌研究领域的紧迫课题。本研究在系统探讨核因子E2相关因子2（nuclear factor erythroid 2-related factor 2, Nrf2）促进TNBC进展机制的基础上，进一步评估其在疾病预防领域的潜在应用价值，旨在为TNBC转移的防控提供理论依据。
1　Nrf2调控抗氧化防御机制促进TNBC进展
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肿瘤细胞的快速增殖需要增加代谢率，主要通过线粒体提高能量代谢来维持，从而导致内源性活性氧产生增加[3]。内源性活性氧水平升高，形成持续的氧化应激环境，一旦超过细胞毒性阈值，活性氧诱导的氧化应激将对癌细胞有害，并导致细胞凋亡或衰老。因此，癌细胞通过增强抗氧化防御机制来适应高活性氧浓度。Nrf2由 NFE2L2 基因编码，是一种参与细胞防御氧化应激的转录激活因子。正常条件下，Nrf2 处于低水平，Nrf2被负调节因子-氧化应激相关蛋白（kelch-like ECH-associated protein 1，Keap1） 通过泛素-蛋白酶体途径降解[4]。然而，在亲电或氧化应激下，Keap1 改变结构，Nrf2 从复合物中解离，在细胞核中积累，识别并结合抗氧化反应元件（antioxidant response element, ARE），启动还原型烟酰胺腺嘌呤二核苷酸磷酸[reduced nicotinamide adenine dinucleotide phosphate，NAD（P）H]:醌氧化还原酶1（quinone oxidoreductase 1,NQO1）、血红素加氧酶-1（heme oxygenase-1，HO-1）、谷氨酸-半胱氨酸连接酶催化亚基（glutamate-cysteine ligase catalytic subunit，GCLC）等多种Ⅱ相解毒酶和抗氧化蛋白的转录[5-6]，并诱导其参与抗氧化反应、代谢和炎症的靶基因表达[7]。因此 Keap1-Nrf2通路是肿瘤细胞防御氧化损伤的核心机制。有研究发现乳腺癌所有细胞系中均检测出Nrf2，在细胞质和细胞核中均有表达，而且细胞核内的表达水平更高[8]。在所有类型的乳腺癌细胞中，不论肿瘤大小均有Nrf2蛋白表达，说明Nrf2介导的氧化应激过程持续于各种乳腺癌类型的所有阶段[9]，在乳腺癌特别是 TNBC 中高 Nrf2 水平和（或）Keap1的低表达，与患者的总生存期和无病生存期显著缩短呈强相关[10]。Nrf2信号通路是乳腺癌抗氧化应激的主要防御机制，也是肿瘤进展的显著标志[11]。有研究表明，乳腺癌干细胞通过Keap1-Nrf2信号通路增强其抗氧化防御，从而增加治疗抵抗性[12]。有学者建议将Nrf2作为乳腺癌的治疗靶点[13]。用Nrf2抑制剂-维生素C处理乳腺癌细胞后，Nrf2 mRNA和蛋白水平均显著降低。MDA-MB-231细胞中的核/胞质Nrf2比例降低了1.7倍，在MDA-MB 468细胞中降低了2倍，在MCF-7细胞中降低了1.4倍，在A549细胞中降低了1.2倍。治疗结果表明，维生素C以剂量依赖性方式减少内源性活性氧的生成(P=0.027)。研究表明维生素C 治疗可作为Nrf2过表达患者的辅助治疗方法[14]。然而目前TNBC细胞异质性的复杂性和Nrf2作用仍在广泛研究中，现有数据表明Nrf2在乳腺癌尤其是TNBC进展中的重要性仍然有限[15]。
2　Nrf2调控TNBC铁死亡防御系统促进TNBC进展
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TNBC具有铁和脂质代谢异常的特征，故对铁死亡尤为敏感。铁死亡是一种铁依赖的、由脂质过氧化引起的新型细胞死亡模式，其核心特征是由细胞内芬顿反应产生的脂质活性氧的致命性蓄积、谷胱甘肽水平降低以及谷胱甘肽过氧化物酶4（glutathione peroxidase 4，GPX4）活性降低，当执行铁死亡的活性物质超过细胞自身抗氧化能力时就会发生铁死亡[16]。癌细胞通过抵抗铁死亡信号增强抗氧化防御机制，抑制铁死亡并避免细胞死亡，这种防御机制构成了细胞的铁死亡防御体系。在细胞铁死亡防御系统中，Nrf2被视为主调控因子，是TNBC细胞中主要的抗铁死亡介质，通过调节ARE，包括NQO1和FTH等基因，进一步调控抗铁死亡基因特别是SLC7A11和GPX4这两个核心抗铁死亡基因的转录，防止并纠正导致铁死亡的氧化还原失衡[17-18]。然而，癌细胞通过提升Nrf2解毒程序的基础表达水平，以对抗细胞内活性氧，从而维持原平衡状态的细胞环境[19]。因此，Nrf2被证实是预防过氧化和铁死亡的关键调控因子，其作用机制可对抗铁死亡驱动的抗癌疗法疗效，并增强细胞对铁死亡的抵抗能力[20]。相反，Nrf2不足会抑制多种Nrf2靶点的活性，从而触发铁死亡进程，或使癌细胞对铁死亡诱导剂更易敏感，为铁死亡癌症治疗提供了极具潜力的药物靶点[21]。诱导铁死亡可能成为TNBC治疗和预防新策略。有研究证实了Nrf2与GPX4信号传递，完整呈现了STAT3-SIRT3-Nrf2-GPX4信号链路[22]，阐明天然二萜毛萼乙素（eriocalyxin B，Eri B）通过抑制 STAT3 依赖的SIRT3转录，级联下调抗氧化关键因子Nrf2与GPX4，从而特异性放大铁死亡信号。最新研究显示，在TNBC的Luminal雄激素受体亚型中，GPX4抑制剂联合免疫检查点阻滞剂的联合疗法，相比单药治疗能显著抑制肿瘤生长[23]。在TNBC肿瘤中，自噬功能失调是常见现象，p62介导的Nrf2持续激活是促进肿瘤进展的另一重要途径[24]。有研究构建模拟三磷酸腺苷酶（adenosine triphosphatase，ATP）活性的碳化钒MXene纳米酶（PVCMs），可以有效地将ATP去磷酸化为二磷酸稂苷（adenosine diphosphate，ADP）并降低细胞内能量状态，从而通过p62-Keap1-Nrf2轴诱导自噬，从而抑制TNBC细胞中的Nrf2抗氧化程序。因此，PVCM可以抑制 Nrf2 防御系统并消耗谷胱甘肽，通过细胞内内源性铁介导的 Fenton 反应驱动铁死亡、TNBC 细胞死亡[25]。有研究采用PRMT5 选择性甲基化 Keap1，通过Nrf2/HMOX1 轴，抑制Nrf2活性，下调HMOX1的表达，从而抵制 TNBC细胞铁死亡[26]。
3　Nrf2通过代谢重编程促进TNBC进展
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代谢重编程是TNBC进展的核心驱动力之一[27]。与其他乳腺癌亚型相比，TNBC细胞表现出更强的葡萄糖摄取能力和更高的糖酵解基因/蛋白表达水平，呈现出典型的“瓦博格效应”（Warburg effect）[28]，该代谢模式不仅为肿瘤细胞提供了快速生成ATP的途径，更重要的是，它将代谢中间产物分流至各项生物合成途径，为细胞的快速增殖提供了物质基础。研究表明，TNBC细胞除了依赖经典的氧化应激诱导激活模式外，可通过一种独特的、不依赖氧化应激的机制激活Nrf2,细胞摄入的半胱氨酸直接与Keap1蛋白上的特定半胱氨酸残基发生共价修饰，从而破坏Keap1对Nrf2的抑制作用，导致Nrf2激活[29]。研究证实，Nrf2启动戊糖磷酸途径（pentose phosphate pathway,PPP),直接结合并激活PPP途径中关键限速酶的基因启动子，包括葡萄糖-6-磷酸脱氢酶（phosphate dehydrogenase,G6PD）和转酮醇酶[30-32]。Nrf2的过表达通过上调G6PD的表达以促进TNBC细胞的增殖[33]。Nrf2可通过与另一关键转录因子（缺氧诱导因子-1α）协同调控TNBC的糖酵解[34]。Nrf2通过上调谷氨酸-半胱氨酸连接酶的两个亚基（催化亚基和调节亚基）调控肿瘤细胞谷胱甘肽的合成[29]。TNBC的脂质代谢存在显著重编码[35]，尚无直接证据表明Nrf2在TNBC中直接调控脂肪酸合成（如FASN,ACC）或脂肪酸氧化（如CPT1）的关键酶，但理论上存在间接调控的可能。Nrf2通过激活PPP途径产生的大量NADPH，是脂肪酸从头合成所必需的还原当量，因此Nrf2的激活可能为脂肪酸合成提供了上游支持。未来需要更深入的研究来阐明Nrf2在TNBC脂质代谢重编程中的确切角色。
4　Nrf2通过调控肿瘤微环境促进TNBC进展
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肿瘤微环境是一个复杂的生态系统，在促进肿瘤进展中扮演者至关重要的作用[36]。肿瘤微环境由肿瘤细胞和非肿瘤细胞组成，涉及多种细胞和分泌因子[37]。TNBC的肿瘤微环境呈现具有较高的肿瘤浸润淋巴细胞比例以及相对较高的程序性死亡配体1（programmed cell death ligand 1，PD-L1）表达水平，然而TNBC的肿瘤微环境存在显著异质性，不同患者的TNBC肿瘤在基因表达、免疫浸润、细胞因子表达存在差异，使得单一的免疫治疗策略难以对所有患者治疗有效[38]。有研究在多种乳腺癌模型（4T1小鼠模型、56S患者来源类器官、MDA-MB-231和HCC70细胞系）中系统评估了Nrf2间接抑制剂—Sulindac对PD-L1表达及免疫检查点阻断疗效的影响。Sulindac显著下调细胞内及外PD-L1表达，通过抑制Stat3信号并上调miR-570-3p实现PD-L1的转录抑制；联合使用Sulindac和抗PD-L1抗体显著提升CD8+T细胞浸润并显著抑制肿瘤体积，结果表明抑制Nrf2能够恢复TNBC对程序性死亡蛋白1（programmed cell death protein 1，PD-1）/PD-L1阻断的治疗敏感性[39]。在MDA-MB-231 TNBC细胞中，天然化合物百里醌处理导致Nrf2蛋白表达升高（>2倍），而PD-L1蛋白表达下降约65%，研究结显示Nrf2活性与PD-L1表达呈显著相关[40]。Nrf2通过上调谷氨酰胺代谢酶和磷酸戊糖途径关键酶，维持肿瘤细胞的还原性代谢状态，间接支持巨噬细胞的M2极化[41]。Nrf2的激活消耗微环境中的胱氨酸等代谢物，进而抑制肿瘤浸润淋巴细胞的功能。Nrf2直接调控VEGF表达，通过HIF-1α间接促进血管新生[42]。Nrf2激活可稳定HIF-1α蛋白，而HIF-1α又能进一步激活Nrf2转录，形成正反馈循环[40]。综上所述，Nrf2均可以影响包括TNBC在内的肿瘤进展。
5　预防医学与公共卫生意义
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5.1　基于Nrf2的早期筛查策略
Nrf2作为TNBC进展的新型分子标志物，在早期筛查中展现出重要价值[43-44]。目前Nrf2的检测方法主要以Western blot、免疫组化、实时定量聚合酶链式反应为主。液体活检技术通过检测外周血中循环肿瘤细胞，可实现对转移风险的动态监测，目前主要聚焦于CK、VIM、CD45等表型标记的检测，有关Nrf2表达水平的检测缺乏直接证据。循环肿瘤DNA已被证实可用于检测乳腺癌微转移[45]。在影像学方面，目前已有针对 HER2的 68Ga 标记单域抗体或 Affibody 进行 PET-CT 成像的临床研究，显示可在同一天完成成像并评估 HER2表达[46]，然而针对 Nrf2 本身的放射性标记抗体（如68Ga-Nrf2）在乳腺癌或 TNBC 中的双模态显像尚未报道。基于人工智能的Nrf2表达预测模型正在开发中，通过整合临床病理特征和基因组数据，可实现对TNBC患者转移风险的个体化评估。
5.2　抗氧化干预策略
在天然化合物中，姜黄素通过共价修饰Keap1的Cys151残基，选择性调节Nrf2活性，其纳米制剂可提高生物利用度3～5倍[47]。雷公藤内酯能够抑制Nrf2信号通路及其下游靶基因的表达，从而提升肿瘤细胞对多柔比星和伊马替尼所诱导的凋亡作用的反应性[48]。白藜芦醇则通过SIRT1介导的Nrf2去乙酰化调控其转录活性，在动物模型中使肺转移灶减少62%[49]。在合成化合物领域，ML385作为首个进入临床试验的Nrf2-DNA结合抑制剂，在Ⅰ期试验中显示出良好的安全性[50]。ML385衍生物K-80003通过靶向Nrf2-MafG相互作用，对TNBC移植瘤的抑制率达71%。最新的研究热点是开发组织特异性Nrf2调节剂，如基于TNBC表面标志物（如EGFR或CD44）的靶向递药系统，可显著提高治疗效果并降低全身毒性[51]。
5.3　公共卫生干预措施
在人群层面，建立基于Nrf2的TNBC防控体系具有重要公共卫生价值。针对高危人群（如BRCA突变携带者），推荐每年进行Nrf2通路基因检测（包括NFE2L2、Keap1和Cul3等），结合蛋白质组学分析，可识别出转移风险升高2～3倍的亚群[29]。在社区防控中，推广“氧化应激-炎症-Nrf2”三位一体的健康管理项目，包括：（1）戒烟干预结合血清8-OHdG（氧化应激标志物）监测；（2）地中海饮食指导，强调摄取富含硫代葡萄糖酸盐（Nrf2天然激活剂）的十字花科蔬菜；（3）定制化运动处方，研究表明适度有氧运动可使Nrf2活性维持生理性波动[52]。医院-社区联动的随访体系也至关重要，对已完成治疗的TNBC患者，建议每3个月检测TNBC中Nrf2靶基因表达谱，其预测复发的灵敏度较传统肿瘤标志物提高40%。此外，针对医疗资源匮乏地区，开发基于干血片的Nrf2快速检测技术，配合移动医疗平台，可实现转移风险的广覆盖筛查。
6　结论与展望
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TNBC一直是乳腺癌研究领域的重点和难点。在分子层面，Nrf2通过调控抗氧化防御机制、铁死亡防御系统促进肿瘤进展；在代谢层面，Nrf2介导的糖酵解增强和谷氨酰胺代谢重编程为转移提供能量支持；在微环境层面，Nrf2通过调节免疫细胞功能和促进血管新生创造适宜转移的微环境。这些发现为理解TNBC的高转移特性提供了新的理论视角。在转化医学方面，基于Nrf2的液体活检技术和分子影像探针的开发有望实现转移的早期预警。靶向Nrf2的干预策略，特别是其抑制剂与免疫治疗、化疗的联合方案已显示出良好的应用前景。未来研究应着重探究Nrf2调控网络的时空特异性、抑制剂的安全给药策略以及精准的患者分层方法。同时，需要开展大规模临床试验验证Nrf2靶向治疗在TNBC全程管理中的价值，并探索其与现有治疗手段的最佳组合方式，从而为改善TNBC患者的预后提供新的突破口。
基金
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  • 国家自然青年科学基金项目(21807041)
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2026年第53卷第1期
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doi: 10.20043/j.cnki.MPM.202507326
  • 接收时间：2025-07-18
  • 首发时间：2026-11-02
  • 出版时间：2026-01-10
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  • 收稿日期：2025-07-18
基金
国家自然青年科学基金项目(21807041)
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    济宁医学院，山东 济宁 272067

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