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Article(id=1239174992789828150, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1239174986137661844, articleNumber=null, orderNo=null, doi=10.14109/j.cnki.xyylc.2024.04.02, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1659283200000, receivedDateStr=2022-08-01, revisedDate=null, revisedDateStr=null, acceptedDate=1692028800000, acceptedDateStr=2023-08-15, onlineDate=1773371941038, onlineDateStr=2026-03-13, pubDate=1713974400000, pubDateStr=2024-04-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1773371941038, onlineIssueDateStr=2026-03-13, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1773371941038, creator=13701087609, updateTime=1773371941038, updator=13701087609, issue=Issue{id=1239174986137661844, tenantId=1146029695717560320, journalId=1205117082300743687, year='2024', volume='43', issue='4', pageStart='241', pageEnd='320', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1773371939453, creator=13701087609, updateTime=1773372128807, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1239175780396233704, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1239174986137661844, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1239175780396233705, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1239174986137661844, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=247, endPage=252, ext={EN=ArticleExt(id=1239174994421412425, articleId=1239174992789828150, tenantId=1146029695717560320, journalId=1205117082300743687, language=EN, title=Research progress of nano-drug delivery system that inhibits signaling pathways in therapy of triple-negative breast cancer, columnId=1207314219599499390, journalTitle=Chinese Journal of New Drugs and Clinical Remedies, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Signaling pathways such as PI3K/AKT/mTOR, Hippo/YAP, Notch, Wnt/β-catenin, and TGF-β play the critical role in the malignant biological behaviors of triple-negative breast cancer（TNBC）, including proliferation, invasion,metastasis, and drug resistance. However, conventional chemotherapy drugs often lead to severe adverse reactions, and the utilization of nanotechnology presents a promising solution to this issue. Nano-drug delivery system based on inhibiting signal transduction pathways can carry conventional chemotherapy drugs, block the proliferation of cancer cells, and impede the progression of TNBC. This approach not only offers advantages in targeted therapy but also reduces tissue damage significantly, giving patients more benefits in the future.

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PI3K/AKT/mTOR、Hippo/YAP、Notch、Wnt/β-catenin、TGF-β等信号传导通路参与了三阴性乳腺癌（TNBC）的增殖、浸润、转移和耐药等恶性生物学行为。常规化疗药物不良反应严重，纳米技术的应用可改善这一状况。基于抑制信号传导通路的纳米递药系统可负载常规化疗药物，高效阻断癌细胞增殖过程，遏制TNBC进展，靶向治疗优势明显，对正常组织的损伤明显减轻，给患者带来更多获益。

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王光辉
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张敏娜，女，副教授，硕士，主要从事纳米材料药物递送系统和药物毒物分析研究，E-mail: 。

王光辉，男，副教授，硕士，主要从事抗肿瘤药物的研究，E-mail:

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张敏娜，女，副教授，硕士，主要从事纳米材料药物递送系统和药物毒物分析研究，E-mail: 。

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张敏娜，女，副教授，硕士，主要从事纳米材料药物递送系统和药物毒物分析研究，E-mail: 。

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王光辉，男，副教授，硕士，主要从事抗肿瘤药物的研究，E-mail:

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王光辉，男，副教授，硕士，主要从事抗肿瘤药物的研究，E-mail:

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抑制信号传导通路的纳米递药系统在三阴性乳腺癌治疗中的研究进展
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张敏娜 , 王光辉
中国新药与临床杂志 | 综述 2024,43(4): 247-252
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中国新药与临床杂志 | 综述 2024, 43(4): 247-252
抑制信号传导通路的纳米递药系统在三阴性乳腺癌治疗中的研究进展
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张敏娜 , 王光辉
作者信息
  • 济宁医学院 药学院，山东 日照　276826

    • 张敏娜，女，副教授，硕士，主要从事纳米材料药物递送系统和药物毒物分析研究，E-mail: 。

    王光辉，男，副教授，硕士，主要从事抗肿瘤药物的研究，E-mail:

通讯作者:

王光辉
Research progress of nano-drug delivery system that inhibits signaling pathways in therapy of triple-negative breast cancer
Min-na ZHANG , Guang-hui WANG
Affiliations
  • College of Pharmacy, Jining Medical Univercity, Rizhao SHANDONG 276826, China
出版时间: 2024-04-25 doi: 10.14109/j.cnki.xyylc.2024.04.02
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摘要
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PI3K/AKT/mTOR、Hippo/YAP、Notch、Wnt/β-catenin、TGF-β等信号传导通路参与了三阴性乳腺癌（TNBC）的增殖、浸润、转移和耐药等恶性生物学行为。常规化疗药物不良反应严重，纳米技术的应用可改善这一状况。基于抑制信号传导通路的纳米递药系统可负载常规化疗药物，高效阻断癌细胞增殖过程，遏制TNBC进展，靶向治疗优势明显，对正常组织的损伤明显减轻，给患者带来更多获益。

三阴性乳腺癌  /  Wnt信号通路  /  纳米颗粒给药系统  /  治疗

Signaling pathways such as PI3K/AKT/mTOR, Hippo/YAP, Notch, Wnt/β-catenin, and TGF-β play the critical role in the malignant biological behaviors of triple-negative breast cancer（TNBC）, including proliferation, invasion,metastasis, and drug resistance. However, conventional chemotherapy drugs often lead to severe adverse reactions, and the utilization of nanotechnology presents a promising solution to this issue. Nano-drug delivery system based on inhibiting signal transduction pathways can carry conventional chemotherapy drugs, block the proliferation of cancer cells, and impede the progression of TNBC. This approach not only offers advantages in targeted therapy but also reduces tissue damage significantly, giving patients more benefits in the future.

triple negative breast neoplasms  /  Wnt signaling pathway  /  nanoparticle drug delivery system  /  therapy
张敏娜, 王光辉. 抑制信号传导通路的纳米递药系统在三阴性乳腺癌治疗中的研究进展. 中国新药与临床杂志, 2024 , 43 (4) : 247 -252 . DOI: 10.14109/j.cnki.xyylc.2024.04.02
Min-na ZHANG, Guang-hui WANG. Research progress of nano-drug delivery system that inhibits signaling pathways in therapy of triple-negative breast cancer[J]. Chinese Journal of New Drugs and Clinical Remedies, 2024 , 43 (4) : 247 -252 . DOI: 10.14109/j.cnki.xyylc.2024.04.02
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浸润性乳腺癌中10% ~ 20%为三阴性乳腺癌（triple-negative breast cancer，TNBC），该恶性肿瘤的生物学行为主要表现为高侵袭性、高转移性和切除后易复发，由于TNBC缺乏明确的药物靶点导致临床治疗困难重重[1，2]。TNBC常规治疗手段有化疗、手术切除、辅助放疗或保乳术后辅助放疗等。到目前为止，化疗仍然是最有效的治疗手段，但化疗药物对正常组织的损伤较大，严重削弱了治疗效果。近年来，研究显示纳米递药系统（nano-drug delivery system）可显著改变化疗药物在体内的生物学活性，其较好的组织相容性可精准识别肿瘤细胞，增加肿瘤细胞对药物的摄取[3，4]。此外，纳米递药系统还可通过光热消融作用消除病灶内的肿瘤细胞，并激活免疫系统，经抗体依赖细胞介导的细胞毒作用（antibody-dependent cell-mediated cytotoxicity，ADCC）杀灭肿瘤细胞[5，6]。近年来相关研究[7，8]表明PI3K/AKT/ mTOR、Hippo/YAP、Notch、Wnt/β-catenin、转化生长因子（TGF）-β、STAT3、ERK-MAPK等信号通路参与TNBC的恶性进展过程，如mTOR信号的过度激活会造成肿瘤细胞的增殖，抑制肿瘤细胞凋亡，促进肿瘤分化，可进一步导致肿瘤的复发或转移；约有80%TNBC患者体内肿瘤细胞Trop-2糖蛋白高表达，拓扑异构酶抑制剂靶向Trop-2糖蛋白，可有效抑制下游ERK-MAPK信号通路的激活；STAT3信号通路参与细胞癌变、分化和肿瘤生长调控。信号传导通路抑制剂成为TNBC治疗的重要研发方向和目标。基于抑制TNBC信号传导通路的纳米递药系统可实施智能化给药，多途径和多靶点抑制肿瘤细胞增殖和代谢，因此在TNBC治疗中具有广泛的应用前景[9，10]。本文介绍近年来纳米递药系统在抑制TNBC信号通路应用方面的研究进展，以期开拓TNBC精准靶向治疗的新思路。
基于PI3K/AKT/mTOR信号通路的纳米递药系统
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PI3K/AKT/mTOR信号通路是多种亚型乳腺癌治疗的靶点，尤其是TNBC。PI3K与表皮生长因子受体（EGFR）结合改变AKT结构，即通过AKT磷酸化调控凋亡和细胞周期相关下游蛋白（cyclin A1、Bax、Bcl-2）活性和mTOR信号蛋白的翻译转录和表达，因此，该信号通路调控肿瘤细胞的分化、增殖以及细胞凋亡过程。PI3K/AKT/mTOR信号通路抑制药物有西妥昔单抗（cetuximab，CTX）、戈沙妥珠单抗（sacituzumab）和德曲妥珠单抗（trastuzumab）。CTX是针对EGFR的单克隆抗体，可抑制肿瘤细胞增殖并诱导其凋亡，以及降低肿瘤新生血管的生成。静脉给药易引发变态反应、骨髓抑制、组织损伤等不良反应，纳米制剂可提高药物治疗的靶向性，进而减少用药后全身组织的不良反应，单克隆抗体对肿瘤细胞受体的高亲和力是实现靶向治疗的基础，由CTX与纳米颗粒共价键偶联形成递药系统，利用胶体纳米颗粒与细胞膜生物大分子在粒径和密度上的相似性，使其更容易被肿瘤细胞捕获进入细胞内，有助于实施对PI3K/AKT/mTOR信号通路的抑制，提高药物的靶向治疗效果。COLOMBO等[11]将CTX的半链（HC-CTX）片段与胶体纳米颗粒共价键偶联形成HC-CTX-NPs，转导进入TNBC细胞株MDA-MB-231进行体外实验，结果显示HC-CTX-NPs能有效干扰下游PI3K/AKT信号通路，抑制肿瘤细胞增殖，促进肿瘤细胞凋亡。进一步通过动物体内实验研究显示，HC-CTX-NPs给药216 h后，肿瘤体积缩小36.56%（CTX对照组肿瘤体积缩小24.32%），治疗过程未见组织损伤等不良反应。另外，治疗过程触发ADCC效应，募集单核细胞、巨噬细胞和自然杀伤细胞，增强了免疫系统对肿瘤细胞的杀灭作用。
PI3K/AKT/mTOR信号抑制剂如PI3K抑制剂、AKT抑制剂、mTOR抑制剂等为TNBC治疗的潜在分子靶点。环氧氮杂二酮纳米递药系统抑制PI3K/AKT信号通路介导的线粒体电位升高，导致TNBC细胞能量缺乏，细胞增殖活力下降，同时抑制肿瘤血管生成，减少环氧合酶2（COX2）、骨桥蛋白（OPN）、血管内皮生长因子（VEGF）和基质金属蛋白酶（MMP）-9等肿瘤转移基因产物的表达，有效遏制肿瘤的增殖和转移[12]。mTOR存在mTORC1和mTORC2两个功能蛋白复合体，可调控肿瘤细胞的能量代谢、增殖和存活。携带mTORC2抑制剂西罗莫司（sirolimus）的纳米递药系统，通过RNA干扰沉默mTOR通路关键基因Rictor基因，经TNBC瘤内注射和静脉注射后均可降低AKT磷酸化水平。HER2蛋白是原癌基因CerbB2（Her2/neu）编码的具有受体酪氨酸激酶（RTK）活性的跨膜糖蛋白，可启动酪氨酸激酶调控的信号系统[13]。西罗莫司纳米递药系统与HER2抑制剂拉帕替尼（lapatinib）联合使用，在TNBC动物模型中可进一步降低肿瘤细胞AKT磷酸化水平，使肿瘤生长速度减慢，肿瘤体积缩小44.56%，抑制肿瘤细胞增殖效果明显[13]。总之，PI3K/AKT/mTOR信号通路抑制剂借助纳米递药系统有望实现双重或多重抑制效应。此外，纳米材料可作为近红外光触发剂的载体，在肿瘤病灶继发产生活性氧，高浓度活性氧破坏细胞膜和生物大分子，对肿瘤细胞有一定的杀伤作用，为TNBC靶向治疗带来了更良好的前景。
基于Hippo/YAP信号通路的纳米递药系统
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肿瘤干细胞（CSCs）是随时启动进入增殖周期的细胞亚群，是肿瘤复发和频繁转移的根源，也是TNBC细胞难以根除的主要因素。转录共调节因子YAP和TAZ与转录因子TEAD相配合，共同维持肿瘤细胞增殖、抑制凋亡、维持CSCs属性、诱导肿瘤血管生成、抑制免疫反应并参与了肿瘤耐药过程。目前，紫杉醇（PTX）、多柔比星（DOX）等为主的化疗药物仍然是系统治疗的主要手段。EL-SAHLI等[14]研究发现，PTX、维替泊芬和康美他汀（CA4）共载纳米递药系统，不仅有效抑制TNBC细胞活力，减少肿瘤细胞迁移，而且还显著减少PTX诱导和/或CA4诱导的CSCs富集，进一步的实验揭示其治疗机制与抑制TNBC中上调的Hippo/YAP信号分子有关，该共载纳米递药系统能有效抑制肿瘤细胞、CSCs增殖和肿瘤血管形成。
纳米金（AuNPs）粒径13 nm左右，具有高电子密度、介电特性和催化作用，能选择性地与肿瘤细胞膜上蛋白质大分子结合进入肿瘤细胞内部。AuNPs借助pH敏感的酰胺键结合到多西紫杉醇纳米载体，可有效阻止肿瘤外正常组织细胞的摄取，借助纳米材料的拉曼散射光谱效应来实施药物释放监测。AuNPs包覆的多孔硅微粒负载多西紫杉醇，除了可以抑制Hippo信号传导外，更突出的特点是在红外线热疗的同时释放多西紫杉醇，可杀死大部分肿瘤细胞和CSCs[15]。
基于Notch信号通路的纳米递药系统
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对体内正常细胞而言，Notch受体及其配体、CSL-DNA结合蛋白和下游靶基因共同构成Notch信号通路，决定各类干细胞分化方向。TNBC细胞过度表达的Notch-1受体和抗凋亡蛋白Bcl-2是信号通路抑制剂的有效靶点。小分子药物ABT-737可抑制Bcl-2增强凋亡信号，是TNBC治疗候选靶向药物，但因其水溶性较差导致疗效欠佳，将ABT-737封装在聚乳酸-共聚乙醇酸纳米颗粒中，并用Notch-1抗体对其功能化，制成了N1-ABT-NPs。该纳米递药系统中的功能化抗体既能特异性结合TNBC细胞，又将Notch-1受体锁定在配体无反应状态，抑制Notch信号通路，上调促凋亡蛋白Noxa（BH3-only家族促凋亡蛋白），诱导肿瘤细胞凋亡，显著增强了ABT-737的细胞凋亡作用，从而有效杀死TNBC细胞。VALCOUKT等[16]的研究结果表明，与非癌性乳腺上皮细胞相比，N1-ABT-NPs可优先结合TNBC细胞，靶向性明显，进一步通过调控Bcl-2和Notch信号，诱导细胞死亡；在小鼠体内实验中，检测到小鼠皮下异种移植瘤中N1-ABT-NPs积聚增加，给药组小鼠存活时间平均为68 d，对照组平均为46 d。
TNBC细胞中存在Notch1受体的过度表达和肿瘤抑制性miR-34a低表达的现象，根据这一思路将miR-34a引入TNBC细胞可有效抑制肿瘤生长，若无有效载体，miR-34a则无法发挥作用。为使miR-34a能够顺利输送到肿瘤细胞，将miR-34a封装在聚乳酸-共聚乙醇酸纳米颗粒中，通过Notch1抗体功能化形成N1-miR34a-NPs。除了结合TNBC细胞表面过度表达的Notch1受体外，N1-miR34a-NPs中的抗体直接抑制Notch信号通路，体外实验证明，N1-miR34a-NPs调节TNBC细胞中的Notch信号和下游miR-34a靶点，诱导肿瘤细胞端粒迅速变短，加剧细胞衰老，同时抑制肿瘤细胞增殖和迁移过程[17]。
基于Wnt信号通路的纳米递药系统
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Wnt信号通路控制细胞生存、增殖、迁移、极性表达和凋亡等过程，在体内稳态被打破时，Wnt信号通路的异常激活参与了TNBC发生、发展。Wnt信号驱动肿瘤细胞的浸润转移，且与肿瘤细胞耐药性的形成有关。抑制Wnt信号通路可导致自噬上调，从而产生耐药性，因此自噬抑制剂与Wnt抑制剂同时应用能提高对TNBC的治疗效果。研究者将自噬抑制剂氯喹（chloroquine）与卷曲蛋白-7（FZD7）抗体涂层纳米壳（FZD7-NS）联合应用于TNBC细胞。FZD7-NS通过阻断Wnt配体和FZD7受体相互作用，从而抑制Wnt信号通路，但自噬标记物蛋白轻链（LC）3的表达增加。FZD7-NS和氯喹联合应用可降低TNBC细胞中干细胞基因的表达，抑制TNBC细胞自我更新和转移[18]。SULAIMAN等[19]构建一种PTX和维替泊芬共载的纳米颗粒（PV-NPs），靶向作用于TNBC患者来源的异种移植瘤（patient-derived xenograft，PDX）和CSCs。在PDX小鼠模型实验中，与游离药物相比，PV-NPs显著抑制PDX的生长，同时抑制NF-κB、Wnt和YAP信号通路，在消除TNBC细胞和CSCs方面显示出协同效应[19]。
基于TGF-β信号通路的纳米递药系统
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TGF-β信号参与机体内环境稳态的维持、早期胚胎发育等过程。TGF-β信号通路的异常与胚胎发育异常、肿瘤、组织纤维化、心血管疾病和免疫性疾病等有关[20]。TGF-β抑制剂调节肿瘤异常机械微环境以增强光敏剂的释放是治疗富含间质实体瘤的有效策略[21]。光动力疗法（photodynamic therapy，PDT）是临床上常用的癌症治疗方法，肿瘤血管异常机械微环境在一定程度上不利于PDT的实施，实体瘤中肿瘤间质细胞含量增加积累的固体应力使肿瘤血管受压迫，而光敏剂在肿瘤组织中依赖血液传送，制约了光敏剂的应用。CHEN等[22]通过一步酯化方法合成羟乙基淀粉二氢卟吩e6（HES-Ce6）共轭自组装纳米颗粒（HES-Ce6-NPs），与TGF-β抑制剂LY相结合来增强基于PDT的癌症治疗。LY可减少胶原沉积、减轻固体应力并减压肿瘤血管，重建的肿瘤机械微环境促进HES-Ce6-NPs在肿瘤组织中的积累和渗透，增强HES-Ce6-NPs介导的PDT杀灭肿瘤细胞的功能，在660 nm激光照射下，光稳定性增强，产生的活性氧的量明显多于游离Ce6。
基因治疗可能是改善TNBC预后的更有效策略。胸腺肽反义转录物1（TMPO-AS1）是一种增殖相关的致癌长链非编码RNA（lncRNA），通过稳定雌激素受体-α mRNA促进激素依赖性乳腺癌的进展，可改变TGF-β信号通路相关基因特征。癌症基因组图谱中的转录组数据及TNBC细胞系和患者来源细胞中的转录组数据均显示，TMPO-AS1在基底样乳腺癌亚型中大量表达。基于siRNA功能缺失分析表明，TMPO-AS1基因敲除显著抑制TNBC细胞的增殖和迁移。MITOBE等[23]应用纳米工程技术构造药物递送系统对TMPO-AS1靶向siRNA进行治疗，可显著抑制原发性和转移性TNBC PDX的体内生长。将含有25核苷酸的miRNA正义链通过沉默基因Slug封装在DSPE-PEG2000-tLyp-1肽修饰的纳米级功能脂质体中构成递药系统，用来评估miRNA脂质体对侵袭性TNBC细胞和荷瘤裸鼠的疗效。体外实验结果显示该体系被TNBC细胞有效捕获并靶向线粒体，可抑制Slug蛋白和基因的表达，抑制TNBC中TGF-β/Smad通路，肿瘤细胞的侵袭性和生长速度明显降低；在体内实验中，该体系显著增加了荷瘤裸鼠血液中药物的半衰期，并增加了药物在乳腺癌组织中的积累；功能性miRNA脂质体不影响体重，治疗中未见组织器官损伤[24]。
基于NF-κB信号通路的纳米递药系统
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在TNBC发生过程中，NF-κB的持续激活导致与细胞周期相关的蛋白活性异常增高，进一步导致肿瘤细胞生长失控及肿瘤的浸润和转移。此外，肿瘤血管的形成和肿瘤细胞抗凋亡机制等都与其密切相关。抑制NF-κB的活性，进一步抑制DNA活化，可控制TNBC细胞增殖。研究[25]显示，DOX-透明质酸超顺磁性氧化铁纳米颗粒（DOX-HA-SPION-NPs）递药系统在TNBC细胞株MDA-MB-231中显示出较好的治疗效果。通过共聚焦显微镜检测到细胞质对DOX-HA-SPION的摄取量超过游离DOX，与DOX相比，DOX-HA-SPION能增强细胞凋亡，显著降低促炎性细胞因子IL-6和NF-κB的水平，在治疗转移性和化疗耐药的TNBC方面显示出了良好的潜力。
PTX抗肿瘤机制为诱导微管蛋白形成稳定微管，抑制纺锤体和纺锤丝形成，PTX药物毒性包括骨髓抑制、心血管毒性、神经毒性等，PTX在纳米递药系统中可有效阻断肿瘤增殖信号。在观察PTX联合补骨脂素聚合物脂质纳米粒PSO-PLNs抗TNBC的实验中，与对照组相比，PTX-PSO-PLNs组TNBC细胞凋亡明显增加，磷酸化IRAK1和NF-κB介导的肿瘤细胞的迁移、侵袭减少，对肿瘤生长和肺转移有明显抑制作用，治疗过程未见明显的组织毒性[26]。UC003XSL.1是一种新型lncRNA，在TNBC中高表达，并与TNBC患者的不良预后相关。UC003XSL.1可直接与NF-κB抑制因子（NKRF）结合，阻止NKRF与NF-κB应答基因IL-8启动子中的负调控元件结合，消除了NKRF对NF-κB介导的IL-8转录的负调控，激活的NF-κB/IL-8轴促进了TNBC的进展。XU等[27]研发了一种人滋养细胞表面抗原2（TROP2）靶向的氧化还原反应纳米颗粒（redox-responsive nanoparticle，RR-Np），将UC003XSL.1 siRNA导入体内TNBC细胞，靶向UC003XSL.1阻断了NF-κB/IL-8轴激活，抑制了TNBC的生长和转移。
总结与展望
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纳米递药系统在TNBC治疗中体现出来的优势包括：（1）纳米递药系统通过单种类或多种类药物缓释效应发挥对TNBC细胞及CSCs相关信号通路的持续抑制作用[28，29]。（2）纳米载体携带药物突破血脑屏障、血眼屏障及细胞生物膜屏障，聚集于肿瘤病灶，提高了药物的生物利用度，明显改善了药物的药动学和药效学。（3）纳米递药系统集高效性、低毒性和精准靶向性于一体，智能化给药，多途径、多靶点抑制肿瘤细胞增殖、转移和肿瘤复发[30，31]。总的来说，纳米递药系统是一种具有巨大潜力的药物递送系统，通过抑制PI3K/AKT/mTOR、Notch、Hippo/YAP、Wnt/β-catenin、TGF-β等信号通路，有效遏制TNBC肿瘤细胞的增殖、复发和耐药[32-35]。随着纳米技术的不断进步和应用范围的不断扩大，纳米递药系统将在未来的药物研究中发挥更加重要的作用。
基金
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  • 山东省中医药科技发展计划项目(2019-0453)
  • 济宁市科技发展计划项目(2019SMNS028)
文献
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2024年第43卷第4期
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doi: 10.14109/j.cnki.xyylc.2024.04.02
  • 接收时间：2022-08-01
  • 首发时间：2026-03-13
  • 出版时间：2024-04-25
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  • 收稿日期：2022-08-01
  • 录用日期：2023-08-15
基金
山东省中医药科技发展计划项目(2019-0453)
济宁市科技发展计划项目(2019SMNS028)
作者信息
    济宁医学院 药学院，山东 日照　276826

通讯作者:

王光辉
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
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红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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