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用于增强铁死亡/凋亡治疗肝细胞癌的乐伐替尼与FePt纳米颗粒的仿生共递送

Biomimetic Co-delivery of Lenvatinib and FePt Nanoparticles for Enhanced Ferroptosis/Apoptosis Treatment of Hepatocellular Carcinoma.

作者信息

Xuan Feichao, Zhao Xingyang, Pang Weiran, Li Zirong, Yin Xiangyi, Xie Weizhong, Zeng Xiaojun, Nie Liming, Yang Junying, Li Shiying, Lai Puxiang, Fang Chihua

机构信息

Department of Hepatobiliary Surgery I, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, China.

Department of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong, 999077, China.

出版信息

Adv Healthc Mater. 2025 Apr;14(11):e2401747. doi: 10.1002/adhm.202401747. Epub 2025 Mar 21.

DOI:10.1002/adhm.202401747
PMID:40114524
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12023810/
Abstract

Lenvatinib, endorse as a first-line targeted therapy, has demonstrated efficacy in extending the survival span of individuals afflicted with advanced Hepatocellular carcinoma (HCC). However, its therapeutic effect wears off with time, which is ascribed to the cancer cell's tendency to evade and tamper with its usual modes of action, severely limiting its clinical use. This study devises an innovative therapeutic modality involving the synergistic co-delivery of FePt nanoparticles (NPs) and Lenvatinib via poly lactic-co-glycolic acid (PLGA) NPs encase in HCC cell membranes (Len/FePt@CMP NPs). The investigation explores the mechanism through which Lenvatinib induces ferroptosis in HCC, notably by dampening the glutathione peroxidase 4 (GPX4) through the inhibition of fibroblast growth factor receptor 4. FePt NPs are engineered to enhance the efficacy of ferroptosis and apoptosis for HCC treatment. Concurrently, the incorporation of the cancer cell membrane facilitates the targeted accumulation of NPs at the tumor site, leveraging mechanisms of immune evasion and homologous targeting. This enhances ferroptosis/apoptosis treatment efficacy, triggeres by Len/FePt@CMP NPs, is convincingly demonstrated both in vitro and in vivo. The proposed approach has the potential to redefine HCC therapeutic paradigms by overcoming mono-therapeutic limitations in current clinical treatments, showcasing the improved efficacy of a comprehensive strategy.

摘要

乐伐替尼被认可为一线靶向治疗药物，已证明在延长晚期肝细胞癌（HCC）患者的生存期方面具有疗效。然而，其治疗效果会随着时间的推移而减弱，这归因于癌细胞逃避和干扰其通常作用方式的倾向，严重限制了其临床应用。本研究设计了一种创新的治疗方式，即通过包裹在肝癌细胞膜中的聚乳酸-乙醇酸共聚物（PLGA）纳米颗粒协同共递送FePt纳米颗粒（NPs）和乐伐替尼（Len/FePt@CMP NPs）。该研究探讨了乐伐替尼诱导肝癌细胞铁死亡的机制，特别是通过抑制成纤维细胞生长因子受体4来抑制谷胱甘肽过氧化物酶4（GPX4）。FePt NPs经过设计，可增强肝癌治疗中铁死亡和凋亡的疗效。同时，癌细胞膜的掺入促进了纳米颗粒在肿瘤部位的靶向积累，利用了免疫逃避和同源靶向机制。Len/FePt@CMP NPs触发的这种增强的铁死亡/凋亡治疗效果在体外和体内均得到了令人信服的证明。所提出的方法有可能通过克服当前临床治疗中的单一治疗局限性来重新定义肝癌治疗模式，展示了综合策略的更高疗效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/4690c9240ff6/ADHM-14-0-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/378b9248e062/ADHM-14-0-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/4198b240eb34/ADHM-14-0-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/4690c9240ff6/ADHM-14-0-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/38012182c322/ADHM-14-0-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/626b6b011354/ADHM-14-0-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/f8aaaf464161/ADHM-14-0-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/e91f0b76f219/ADHM-14-0-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/378b9248e062/ADHM-14-0-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/4357490bc5ca/ADHM-14-0-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/4198b240eb34/ADHM-14-0-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1c0/12023810/4690c9240ff6/ADHM-14-0-g004.jpg

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