Therapeutic Implications of the Drug Resistance Conferred by Extracellular Vesicles Derived from Triple-Negative Breast Cancer Cells - Review

Sep 24, 2026

Anticancer drug resistance blocks effective cancer treatment, and extracellular vesicles (EVs) generated by tumor cells have emerged as a key contributor to resistance, tumor progression, and metastasis. 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.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages21

Reading Time53 min

AccessFree to download

Abstract

Keywords

1. Introduction

Drug resistance types and mechanisms

Triple-negative breast cancer characteristics

Secretome and extracellular vesicles as mediators

EV biogenesis and cargo-mediated communication

2. Therapeutic implications of TNBC-EVs

3. Strategies to overcome TNBC-EV–mediated drug resistance

Review Therapeutic Implications of the Drug Resistance Conferred by Extracellular Vesicles Derived from Triple-Negative Breast Cancer Cells Yong Weon Yi Citation: Yi, Y.W. 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 Academic Editors: Elena Levantini and Daniela Sanchez Bass±res Received: 10 January 2023 Revised: 7 February 2023 Accepted: 10 February 2023 Published: 12 February 2023 Copyright: © 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/)) . Department 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 Abstract: 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. Keywords: anticancer therapeutics; drug resistance; extracellular vesicles; exosomes; triple-negative breast cancer; tumor cell-derived extracellular vesicles 1. Introduction Recent 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] . The 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] . Triple-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

FAQs

Why is anticancer drug resistance considered a major impediment in treatment?

Drug resistance reduces the efficacy of anticancer therapeutics. It also represents an additional challenge to successful cancer care.

What role do extracellular vesicles (EVs) play in drug resistance?

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.

How are EVs categorized and what makes them effective carriers?

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.

Sep 24, 2026

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