CD44-targeted therapy using mP6/Rg3 micelles inhibits oral cancer stem cell proliferation and migration.

IF 5.9 2区医学 Q2 CELL BIOLOGY

Cell Biology and Toxicology Pub Date : 2025-08-01 DOI:10.1007/s10565-025-10070-2

Sijia Cai, Yuwen Chen, Changyu Chen, Ming Liu

{"title":"CD44-targeted therapy using mP6/Rg3 micelles inhibits oral cancer stem cell proliferation and migration.","authors":"Sijia Cai, Yuwen Chen, Changyu Chen, Ming Liu","doi":"10.1007/s10565-025-10070-2","DOIUrl":null,"url":null,"abstract":"Background: This study investigates how mP6/Rg3 micelles modulate ABCB1 expression to induce ferroptosis in oral cancer stem cells (CSC) and enhance oral cancer outcomes.Methods: Micelles targeting CD44 peptide P6 were prepared and characterized using TEM and immunofluorescence. Biocompatibility was evaluated through LIVE/DEAD staining and CCK-8 assays. Impact on oral cancer CSC was assessed through in vitro and OSCC mouse model studies using transcriptomic profiling, proteomic analysis, and metabolomic screening.Results: mP6/Rg3 micelles exhibited good biodegradability, inhibiting CSC proliferation and migration. Integrated multi-omics analysis highlighted ABCB1 as a pivotal modulator in OSCC. Functional assays in cell and animal models validated micelles promote ferroptosis in CSC by inhibiting ABCB1, improving OSCC pathology.Conclusions: Targeting ABCB1 with mP6/Rg3 micelles and regulating CD44 presents a promising approach to suppress oral cancer progression by impacting CSC and tumor metabolic pathways. This study offers crucial molecular insights for new therapeutic strategies in oral cancer treatment.","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"122"},"PeriodicalIF":5.9000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12316819/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Biology and Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10565-025-10070-2","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: This study investigates how mP6/Rg3 micelles modulate ABCB1 expression to induce ferroptosis in oral cancer stem cells (CSC) and enhance oral cancer outcomes.

Methods: Micelles targeting CD44 peptide P6 were prepared and characterized using TEM and immunofluorescence. Biocompatibility was evaluated through LIVE/DEAD staining and CCK-8 assays. Impact on oral cancer CSC was assessed through in vitro and OSCC mouse model studies using transcriptomic profiling, proteomic analysis, and metabolomic screening.

Results: mP6/Rg3 micelles exhibited good biodegradability, inhibiting CSC proliferation and migration. Integrated multi-omics analysis highlighted ABCB1 as a pivotal modulator in OSCC. Functional assays in cell and animal models validated micelles promote ferroptosis in CSC by inhibiting ABCB1, improving OSCC pathology.

Conclusions: Targeting ABCB1 with mP6/Rg3 micelles and regulating CD44 presents a promising approach to suppress oral cancer progression by impacting CSC and tumor metabolic pathways. This study offers crucial molecular insights for new therapeutic strategies in oral cancer treatment.

查看原文本刊更多论文

使用mP6/Rg3胶束的cd44靶向治疗抑制口腔癌干细胞的增殖和迁移。

背景：本研究探讨mP6/Rg3胶束如何调节ABCB1表达诱导口腔癌干细胞（CSC）铁凋亡，并提高口腔癌预后。方法：制备靶向CD44肽P6的胶束，利用透射电镜和免疫荧光技术对其进行表征。通过LIVE/DEAD染色和CCK-8检测评价生物相容性。通过体外和OSCC小鼠模型研究，使用转录组学分析、蛋白质组学分析和代谢组学筛选来评估对口腔癌CSC的影响。结果：mP6/Rg3胶束具有良好的生物降解性，可抑制CSC的增殖和迁移。综合多组学分析表明，ABCB1是OSCC的关键调节因子。细胞和动物模型的功能分析证实，胶束通过抑制ABCB1促进CSC中的铁凋亡，改善OSCC病理。结论：mP6/Rg3胶束靶向ABCB1并调控CD44是通过影响CSC和肿瘤代谢途径抑制口腔癌进展的一种有前景的方法。这项研究为口腔癌治疗的新策略提供了重要的分子见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Cell Biology and Toxicology 生物-毒理学

CiteScore

9.90

自引率

4.90%

发文量

101

审稿时长

>12 weeks

期刊介绍： Cell Biology and Toxicology (CBT) is an international journal focused on clinical and translational research with an emphasis on molecular and cell biology, genetic and epigenetic heterogeneity, drug discovery and development, and molecular pharmacology and toxicology. CBT has a disease-specific scope prioritizing publications on gene and protein-based regulation, intracellular signaling pathway dysfunction, cell type-specific function, and systems in biomedicine in drug discovery and development. CBT publishes original articles with outstanding, innovative and significant findings, important reviews on recent research advances and issues of high current interest, opinion articles of leading edge science, and rapid communication or reports, on molecular mechanisms and therapies in diseases.