Eguchi Takanori, Taha Eman Ahmed, Calderwood Stuart K, Ono Kisho
Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8525, Japan.
Advanced Research Center for Oral and Craniofacial Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8525, Japan.
Biology (Basel). 2020 Mar 5;9(3):47. doi: 10.3390/biology9030047.
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).
细胞外囊泡（EVs），如外泌体或肿瘤小体，通常携带源自肿瘤细胞的致癌分子。此外，越来越多的证据表明，肿瘤细胞可以将化疗药物和靶向药物等抗癌药物包裹在细胞外囊泡中排出，这是一种新的耐药机制。释放细胞外囊泡的耐药表型通常与经历上皮-间质转化（EMT）的细胞中的细胞去分化和转化以及癌症干细胞表型的形成有关。细胞外囊泡的释放也参与免疫抑制。在此，我们探讨细胞外囊泡调节肿瘤微环境以对抗癌药物和基于抗体的药物产生耐药性的不同方面，以及耐药相关分泌表型（RASP）的概念。
