The enhanced treatment efficacy of invasive brain glioma by dual-targeted artemether plus paclitaxel micelles

AbstractHigh grade-gliomas are highly invasive and prone to metastasis, leading to poor survival and prognosis. Currently, we urgently need a new treatment strategy to effectively inhibit glioma. In this study, artemether and paclitaxel were used as two agents for tumour suppression. Two functional...

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Bibliographic Details
Main Authors: Xiuying Li, Luanxia Shi, Yandong Li, Qinqing Li, Xiujun Duan, Yingli Wang, Qingshan Li
Format: Article
Language:English
Published: Taylor & Francis Group 2020-01-01
Series:Artificial Cells, Nanomedicine, and Biotechnology
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Online Access:https://www.tandfonline.com/doi/10.1080/21691401.2020.1773489
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Summary:AbstractHigh grade-gliomas are highly invasive and prone to metastasis, leading to poor survival and prognosis. Currently, we urgently need a new treatment strategy to effectively inhibit glioma. In this study, artemether and paclitaxel were used as two agents for tumour suppression. Two functional materials were synthesised and modified on the surface of the micelle as targeting molecules. The addition of two functional materials confers the ability of the micelles to effectively cross the blood-brain barrier (BBB) and then target the glioma cells. Thus, this dual-targeted delivery system allows the drug to play a better role in inhibiting tumour invasion and vasculogenic mimicry (VM) channels. In this paper, the anticancer effects of dual-targeted artemether plus paclitaxel micelles on glioma U87 cells were studied in three aspects: (I) In vitro and in vivo targeting assessment, including the role of penetrating BBB and targeting glioma; (II) In vitro regulation of invasion-associated proteins; (III) Inhibition of VM channels formation and invasion in vitro; (IV) The study of pharmacodynamics in tumour-bearing mice. These results suggest that dual-targeted artemether plus paclitaxel micelle may provide a new strategy to treat glioma via inhibiting invasive and VM channels.
ISSN:2169-1401
2169-141X