Therapy-induced chemoexosomes: Sinister small extracellular vesicles that support tumor survival and progression.
Therapy-induced chemoexosomes: Sinister small extracellular vesicles that support tumor survival and progression.
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治疗诱导的化学外泌体：支持肿瘤存活和进展的险恶的小细胞外囊泡。
DOI：
10.1016/j.canlet.2020.08.022
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发表时间：
2020-11-28
期刊：
影响因子：
9.7
通讯作者：
Sanderson RD
中科院分区：
文献类型：
--
作者：
Bandari SK;Tripathi K;Rangarajan S;Sanderson RD
化疗涉及使用多种细胞毒性或细胞生长抑制药物，通过各种机制杀死或阻止癌细胞的生长。化疗仍然是控制癌症最常用的方法。新出现的证据表明，癌细胞激活各种促生存机制，以科普化疗压力。这些机制在治疗期间持续存在，通常有助于协调肿瘤再生和患者复发。外泌体由于其携带和转移多种生物活性组分的性质而成为癌症发病机制中的关键参与者。最近的数据表明，化疗应激增强分泌并改变外泌体携带的货物。这些改变的外泌体，我们称之为化学外泌体，能够将货物转移到靶肿瘤细胞，这可以增强它们的化学抗性，增加它们的转移行为，在某些情况下甚至有助于赋予肿瘤细胞癌症干细胞样特性。这篇简短的综述总结了我们对化学外泌体对肿瘤生存和进展的影响的理解的最新进展。
Chemotherapy involves the use of multiple cytotoxic or cytostatic drugs acting by various mechanisms to kill or arrest the growth of cancer cells. Chemotherapy remains the most utilized approach for controlling cancer. Emerging evidence indicates that cancer cells activate various pro-survival mechanisms to cope with chemotherapeutic stress. These mechanisms persist during treatment and often help orchestrate tumor regrowth and patient relapse. Exosomes due to their nature of carrying and transferring multiple biologically active components have emerged as key players in cancer pathogenesis. Recent data demonstrates that chemotherapeutic stress enhances the secretion and alters the cargo carried by exosomes. These altered exosomes, which we refer to as chemoexosomes, are capable of transferring cargo to target tumor cells that can enhance their chemoresistance, increase their metastatic behavior and in certain cases even aid in endowing tumor cells with cancer stem cell-like properties. This mini-review summarizes the recent developments in our understanding of the impact chemoexosomes have on tumor survival and progression.
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影响因子：
37.3
作者：
Koumangoye RB;Nangami GN;Thompson PD;Agboto VK;Ochieng J;Sakwe AM
通讯作者：
Sakwe AM
DOI：
10.1186/s13058-016-0740-2
发表时间：
2016-08-11
期刊：
Breast cancer research : BCR
影响因子：
--
作者：
Bussard KM;Mutkus L;Stumpf K;Gomez-Manzano C;Marini FC
通讯作者：
Marini FC
影响因子：
2.8
作者：
Field-Smith A;Morgan GJ;Davies FE
通讯作者：
Davies FE
影响因子：
78.5
作者：
Chabner, BA;Roberts, TG
通讯作者：
Roberts, TG
肝素酶诱导的骨髓瘤和内皮细胞中Syndecan-1/CD138的脱落会激活VEGFR2和侵入性表型：新型合成蛋白预防。
影响因子：
6.2
作者：
Jung, O.;Trapp-Stamborski, V.;Purushothaman, A.;Jin, H.;Wang, H.;Sanderson, R. D.;Rapraeger, A. C.
通讯作者：
Rapraeger, A. C.