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Methadone-mediated sensitization of glioblastoma cells is drug and cell line dependent

机译:美沙酮介导的胶质细胞瘤细胞的致敏是药物和细胞系依赖

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Purpose D,L-methadone (MET), an analgesic drug used for pain treatment and opiate addiction, has achieved attention from oncologists and social media as possible chemoensitizing agent in cancer therapy, notably brain cancer (glioblastoma multiforme, GBM). MET has been reported to enhance doxorubicin-induced cytotoxicity in GBM cells via activation of the mu-opioid receptor (MOR). Here, we extended this work and quantified the toxic effect of MET in comparison to other opioids alone and in combination with doxorubicin and the clinically more relevant alkylating drug temozolomide (TMZ), using a set of GBM cell lines and primary GBM cells.
机译:目的D,L-美沙酮(MET),一种用于疼痛治疗和阿片成瘾的止痛药,作为癌症治疗中可能的化学增敏剂,已引起肿瘤学家和社交媒体的关注,尤其是脑癌(多形性胶质母细胞瘤,GBM)。据报道,MET通过激活mu阿片受体(MOR)增强阿霉素诱导的GBM细胞毒性。在此,我们利用一组GBM细胞系和原代GBM细胞,扩展了这项工作,并量化了MET与其他阿片类药物单独或与阿霉素和临床上更相关的烷基化药物替莫唑胺(TMZ)联合使用时的毒性作用。

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