A novel model of cancer drug resistance: oncosomal release of cytotoxic and antibody-based drugs

Takanori Eguchi; Eman Ahmed Taha; Stuart K. Calderwood; Kisho Ono

doi:10.3390/biology9030047

A novel model of cancer drug resistance: oncosomal release of cytotoxic and antibody-based drugs

Takanori Eguchi, Eman Ahmed Taha, Stuart K. Calderwood, Kisho Ono

Research output: Contribution to journal › Review article

Abstract

Extracellular vesicles (EVs), such as exosomes or oncosomes, often carry oncogenic molecules derived from tumor cells. In addition, accumulating evidence indicates that tumor cells can eject anti-cancer drugs such as chemotherapeutics and targeted drugs within EVs, a novel mechanism of drug resistance. The EV-releasing drug resistance phenotype is often coupled with cellular dedifferentiation and transformation in cells undergoing epithelial-mesenchymal transition (EMT), and the adoption of a cancer stem cell phenotype. The release of EVs is also involved in immunosuppression. Herein, we address different aspects by which EVs modulate the tumor microenvironment to become resistant to anticancer and antibody-based drugs, as well as the concept of the resistance-associated secretory phenotype (RASP).

Original language	English
Article number	47
Journal	Biology
Volume	9
Issue number	3
DOIs	https://doi.org/10.3390/biology9030047
Publication status	Published - Mar 2020

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Keywords

Acidosis
Cell stress response
Drug resistance
Epithelial-mesenchymal transition (EMT)
Exosome
Extracellular vesicle (EV)
Heat shock protein (HSP)
Hypoxia
Oncosome
Resistance-associated secretory phenotype (RASP)
Tumor immunology

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)
Immunology and Microbiology(all)
Agricultural and Biological Sciences(all)

Cite this

Eguchi, T., Taha, E. A., Calderwood, S. K., & Ono, K. (2020). A novel model of cancer drug resistance: oncosomal release of cytotoxic and antibody-based drugs. Biology, 9(3), [47]. https://doi.org/10.3390/biology9030047

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abstract = "Extracellular vesicles (EVs), such as exosomes or oncosomes, often carry oncogenic molecules derived from tumor cells. In addition, accumulating evidence indicates that tumor cells can eject anti-cancer drugs such as chemotherapeutics and targeted drugs within EVs, a novel mechanism of drug resistance. The EV-releasing drug resistance phenotype is often coupled with cellular dedifferentiation and transformation in cells undergoing epithelial-mesenchymal transition (EMT), and the adoption of a cancer stem cell phenotype. The release of EVs is also involved in immunosuppression. Herein, we address different aspects by which EVs modulate the tumor microenvironment to become resistant to anticancer and antibody-based drugs, as well as the concept of the resistance-associated secretory phenotype (RASP).",

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AB - Extracellular vesicles (EVs), such as exosomes or oncosomes, often carry oncogenic molecules derived from tumor cells. In addition, accumulating evidence indicates that tumor cells can eject anti-cancer drugs such as chemotherapeutics and targeted drugs within EVs, a novel mechanism of drug resistance. The EV-releasing drug resistance phenotype is often coupled with cellular dedifferentiation and transformation in cells undergoing epithelial-mesenchymal transition (EMT), and the adoption of a cancer stem cell phenotype. The release of EVs is also involved in immunosuppression. Herein, we address different aspects by which EVs modulate the tumor microenvironment to become resistant to anticancer and antibody-based drugs, as well as the concept of the resistance-associated secretory phenotype (RASP).

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Access to Document

10.3390/biology9030047