{"title":"Bone marrow mesenchymal stem cell derived exosomal miR-361-5p reversed the effect of bortezomib on multiple myeloma.","authors":"Tianbao Lin, Yun Zhang, Zhiping Hu, Shuyan Liu","doi":"10.1177/09287329251350918","DOIUrl":null,"url":null,"abstract":"<p><p>BackgroundBortezomib is the first-line drug in the treatment of multiple myeloma (MM) and its resistance is the main obstacle to cure MM. MicroRNA-361-5p (MiRNA-361-5p) in bone marrow mesenchymal stem cells (BMSCs) might participate in the bortezomib resistance via paracrine pathway. The study was to characterize the role and molecular mechanism of miR-361-5p in bortezomib resistance in MM.MethodsThe exosomes of BMSCs were obtained and characterized by transmission electron microscopy and nanoparticle tracking analysis. The MM cell U266 was treated with bortezomib, bortezomib and BMSC exosomes, bortezomib and BMSC exosomes transfected with miR-361-5p inhibitor. The cell viability was measured by cell counting kit. Protein expression of PDPK1, PI3K, p-PI3K, mTOR, p-mTOR, AKT, and Pan-AKT was detected by western blot. The apoptosis level of bortezomib resistant cell lines was detected by flow cytometry.ResultsLow expression of miR-361-5p promoted the survival of U266 cells and inhibited cell apoptosis, reversing the inhibitory effect of bortezomib on U266 cells. PDPK1 may be a downstream target of miR-361-5p. Low expression of BMSCs-derived exosomal miR-361-5p may reverse the effect of bortezomib on U266 cells by regulating the PDPK1/PI3K/AKT/mTOR axis.ConclusionLow expression of BMSCs-derived exosomal miR-361-5p may overcome bortezomib resistance in MM by regulating PDPK1/PI3K/AKT/mTOR axis.</p>","PeriodicalId":48978,"journal":{"name":"Technology and Health Care","volume":" ","pages":"9287329251350918"},"PeriodicalIF":1.8000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Technology and Health Care","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1177/09287329251350918","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ENGINEERING, BIOMEDICAL","Score":null,"Total":0}
引用次数: 0
Abstract
BackgroundBortezomib is the first-line drug in the treatment of multiple myeloma (MM) and its resistance is the main obstacle to cure MM. MicroRNA-361-5p (MiRNA-361-5p) in bone marrow mesenchymal stem cells (BMSCs) might participate in the bortezomib resistance via paracrine pathway. The study was to characterize the role and molecular mechanism of miR-361-5p in bortezomib resistance in MM.MethodsThe exosomes of BMSCs were obtained and characterized by transmission electron microscopy and nanoparticle tracking analysis. The MM cell U266 was treated with bortezomib, bortezomib and BMSC exosomes, bortezomib and BMSC exosomes transfected with miR-361-5p inhibitor. The cell viability was measured by cell counting kit. Protein expression of PDPK1, PI3K, p-PI3K, mTOR, p-mTOR, AKT, and Pan-AKT was detected by western blot. The apoptosis level of bortezomib resistant cell lines was detected by flow cytometry.ResultsLow expression of miR-361-5p promoted the survival of U266 cells and inhibited cell apoptosis, reversing the inhibitory effect of bortezomib on U266 cells. PDPK1 may be a downstream target of miR-361-5p. Low expression of BMSCs-derived exosomal miR-361-5p may reverse the effect of bortezomib on U266 cells by regulating the PDPK1/PI3K/AKT/mTOR axis.ConclusionLow expression of BMSCs-derived exosomal miR-361-5p may overcome bortezomib resistance in MM by regulating PDPK1/PI3K/AKT/mTOR axis.
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Technology and Health Care is intended to serve as a forum for the presentation of original articles and technical notes, observing rigorous scientific standards. Furthermore, upon invitation, reviews, tutorials, discussion papers and minisymposia are featured. The main focus of THC is related to the overlapping areas of engineering and medicine. The following types of contributions are considered:
1.Original articles: New concepts, procedures and devices associated with the use of technology in medical research and clinical practice are presented to a readership with a widespread background in engineering and/or medicine. In particular, the clinical benefit deriving from the application of engineering methods and devices in clinical medicine should be demonstrated. Typically, full length original contributions have a length of 4000 words, thereby taking duly into account figures and tables.
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Reviews and Tutorials (upon invitation only): Tutorial and educational articles for persons with a primarily medical background on principles of engineering with particular significance for biomedical applications and vice versa are presented. The Editorial Board is responsible for the selection of topics.
4.Minisymposia (upon invitation only): Under the leadership of a Special Editor, controversial or important issues relating to health care are highlighted and discussed by various authors.
5.Letters to the Editors: Discussions or short statements (not indexed).
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