TY - JOUR
T1 - A novel model of cancer drug resistance
T2 - oncosomal release of cytotoxic and antibody-based drugs
AU - Eguchi, Takanori
AU - Taha, Eman Ahmed
AU - Calderwood, Stuart K.
AU - Ono, Kisho
N1 - Funding Information:
This work was supported by JSPS Kakenhi, grant numbers 17K11642-TE, 19H04051-HO, 19H03817-MT, 18K09789-KN, 17K11643-CS, 17K11669-KOh, and 16K11863-KOn, by Ryobi Teien Memorial Foundation, and by Suzuken Memorial Foundation. E.A.T. was supported by the Egypt-Japan Education Partnership (EJEP) grant. Acknowledgments: We thank Akira Sasaki, Ayano Satoh, and Kuniaki Okamoto for mentorship support and Chiharu Sogawa, Yuka Okusha, Hotaka Kawai, Keisuke Nakano, and Heiichiro Udono for illuminating discussions.
Publisher Copyright:
© 2020 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2020/3
Y1 - 2020/3
N2 - 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).
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).
KW - Acidosis
KW - Cell stress response
KW - Drug resistance
KW - Epithelial-mesenchymal transition (EMT)
KW - Exosome
KW - Extracellular vesicle (EV)
KW - Heat shock protein (HSP)
KW - Hypoxia
KW - Oncosome
KW - Resistance-associated secretory phenotype (RASP)
KW - Tumor immunology
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U2 - 10.3390/biology9030047
DO - 10.3390/biology9030047
M3 - Review article
AN - SCOPUS:85081234119
VL - 9
JO - Biology
JF - Biology
SN - 2079-7737
IS - 3
M1 - 47
ER -
