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ID 60429
フルテキストURL
fulltext.pdf 1.59 MB
著者
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
抄録
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).
キーワード
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
発行日
2020-03-05
出版物タイトル
Biology
9巻
3号
出版者
MDPI
開始ページ
47
ISSN
2079-7737
資料タイプ
学術雑誌論文
言語
英語
OAI-PMH Set
岡山大学
著作権者
© 2020 by the authors.
論文のバージョン
publisher
PubMed ID
DOI
Web of Science KeyUT
関連URL
isVersionOf https://doi.org/10.3390/biology9030047
ライセンス
http://creativecommons.org/licenses/by/4.0/
助成機関名
日本学術振興会
助成番号
17K11642-TE
19H04051-HO
19H03817-MT
18K09789-KN
17K11643-CS
17K11669-KOh
16K11863-KOn