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ID 60429
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Eguchi, Takanori Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University ORCID Kaken ID publons researchmap
Taha, Eman Ahmed Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Calderwood, Stuart K. Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School
Ono, Kisho Department of Oral and Maxillofacial Surgery, Okayama University Hospital Kaken ID researchmap
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).
Keywords
extracellular vesicle (EV)
exosome
oncosome
drug resistance
epithelial-mesenchymal transition (EMT)
heat shock protein (HSP)
cell stress response
resistance-associated secretory phenotype (RASP)
hypoxia
acidosis
tumor immunology
Published Date
2020-03-05
Publication Title
Biology
Volume
volume9
Issue
issue3
Publisher
MDPI
Start Page
47
ISSN
2079-7737
Content Type
Journal Article
language
英語
OAI-PMH Set
岡山大学
Copyright Holders
© 2020 by the authors.
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publisher
PubMed ID
DOI
Web of Science KeyUT
Related Url
isVersionOf https://doi.org/10.3390/biology9030047
License
http://creativecommons.org/licenses/by/4.0/
Funder Name
Japan Society for the Promotion of Science
助成番号
17K11642-TE
19H04051-HO
19H03817-MT
18K09789-KN
17K11643-CS
17K11669-KOh
16K11863-KOn