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EVs are lipid-bilayer vesicles that transfer proteins, nucleic acids, lipids, and metabolites between cells. Mechanistic understanding of how EVs drive drug resistance remains early, so this review analyzes roles of triple-negative breast cancer–derived EVs (TNBC-EVs) and evaluates strategies to overcome TNBC-EV mediated resistance.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/therapeutic-implications-of-the-drug-resistance-conferred-by-extracellular-vesicles-derived-from-triple-negative-breast-cancer-cells-review/385538/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/therapeutic-implications-of-the-drug-resistance-conferred-by-extracellular-vesicles-derived-from-triple-negative-breast-cancer-cells-review/385538.png","ImageObject",300,407,{"name":92,"@type":93},"pixelkiddo","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-09-27","2026-09-24",true,{"@type":102,"interactionType":103,"userInteractionCount":81},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"Why is anticancer drug resistance considered a major impediment in treatment?","Question",{"text":112,"@type":113},"Drug resistance reduces the efficacy of anticancer therapeutics. 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Therapeutic Implications of the Drug Resistance Conferred by Extracellular Vesicles Derived from Triple-Negative Breast Cancer Cells. Int. J. Mol. Sci. 2023, 24, 3704. [https://doi.org/10.3390/](https://doi.org/10.3390/)[ ](https://doi.org/10.3390/)ijms24043704  \nAcademic Editors: Elena Levantini and Daniela Sanchez Bass±res  \nReceived: 10 January 2023  \nRevised: 7 February 2023  \nAccepted: 10 February 2023  \nPublished: 12 February 2023  \nCopyright: © 2023 by the author. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) .  \nDepartment of Biochemistry, College of Medicine, Dankook University, Cheonan-si 31116, Chungcheongnam-do, Republic of Korea; [yongweon_yi@dankook.ac.kr](yongweon_yi@dankook.ac.kr); Tel.: +82-41-550-3974  \nAbstract: Anticancer drug resistance is a significant impediment in current cancer treatment. Extracellular vesicles (EVs) derived from cancer cells were recently acknowledged as a critical mechanism of drug resistance, tumor progression, and metastasis. EVs are enveloped vesicles comprising a lipid bilayer that transfers various cargo, including proteins, nucleic acids, lipids, and metabolites, from an originating cell to a recipient cell. Investigating the mechanisms whereby EVs confer drug resistance is still in the early stages. In this review, I analyze the roles of EVs derived from triple-negative breast cancer cells (TNBC-EVs) in anticancer drug resistance and discuss strategies to overcome TNBC-EV-mediated drug resistance.  \nKeywords: anticancer therapeutics; drug resistance; extracellular vesicles; exosomes; triple-negative breast cancer; tumor cell-derived extracellular vesicles  \n1. Introduction  \nRecent advances in anticancer drugs have greatly improved cancer patient survival [1,2] . For example, 1 year and 5 year net survival increased between 1995 and 2014, in 3,764,543 eligible cancer cases, and from 19 jurisdictions spanning most cancer types [1] . Survival rate increases are evident in high-income countries. The 5 year mortality rate in adolescents and young adults with primary cancers decreased from 6.8% in those diagnosed between 1975 and 1984 to 4.2% between 2005 and 2011 [2] . These improvements were possible primarily through the development of targeted therapeutics. For example, seventy-one small-molecule protein kinase inhibitors (PKIs) were approved by the US Food and Drug Administration (FDA) as of 29 May 2022 [3]. Over the last thirty-five years, the US FDA has approved 100 monoclonal antibodies for treating various diseases, including cancers [4] . Novel therapeutic modalities, such as chimeric antigen receptor (CAR)-engineered cell therapies and antibody–drug conjugates (ADCs), have also contributed to the overall success of anticancer therapeutics [5–9] .  \nThe emergence of resistance, however, impedes the efficacy of these anticancer therapeutics, and represents another challenge to successful cancer treatment [10] . Two types of drug resistance are intrinsic (de novo or primary), resistance that exists before the use of a drug, and acquired (or secondary), resistance that develops during drug treatment [8,11] . Drug resistance occurs via many mechanisms, including increases in drug efflux, mutations in oncogenes and/or tumor suppressor genes, compensatory survival pathway activations, and DNA damage repair [10,12] .  \nTriple-negative breast cancer (TNBC) is aggressive and accounts for up to 20% of breast cancer types [13–17] . TNBC is characterized by a lack of the expression of hormone receptors, both estrogen (ER) and progesterone (P","cbCaivKOzOwlBgkw","https://ap.wps.com/l/cbCaivKOzOwlBgkw","pdf",1294642,21,"English","# Abstract\n# Keywords\n# 1. Introduction\n## Drug resistance types and mechanisms\n## Triple-negative breast cancer characteristics\n## Secretome and extracellular vesicles as mediators\n## EV biogenesis and cargo-mediated communication\n# 2. Therapeutic implications of TNBC-EVs\n# 3. Strategies to overcome TNBC-EV–mediated drug resistance","[{\"question\":\"Why is anticancer drug resistance considered a major impediment in treatment?\",\"answer\":\"Drug resistance reduces the efficacy of anticancer therapeutics. It also represents an additional challenge to successful cancer care.\"},{\"question\":\"What role do extracellular vesicles (EVs) play in drug resistance?\",\"answer\":\"EVs derived from cancer cells can contribute to drug resistance by transferring diverse cargo between cells. They support tumor progression and metastasis through cell-to-cell communication.\"},{\"question\":\"How are EVs categorized and what makes them effective carriers?\",\"answer\":\"EVs include exosomes, microvesicles (ectosomes), and apoptotic bodies, differing by biogenesis and size. Their lipid bilayer protects vulnerable biomaterials like nucleic acids and growth factors, enabling interactions between distant cells.\"}]","Therapeutic Implications of the Drug Resistance Conferred by Extracellular Vesicles Derived from Triple-Negative Breast Cancer Cells - Review | PDF",1790269875,53]