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本文引用的文献

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Chains of magnetosomes with controlled endotoxin release and partial tumor occupation induce full destruction of intracranial U87-Luc glioma in mice under the application of an alternating magnetic field.在交变磁场的应用下,具有受控内毒素释放和部分肿瘤占据的磁小体链诱导颅内 U87-Luc 神经胶质瘤的完全破坏。
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Development of non-pyrogenic magnetosome minerals coated with poly-l-lysine leading to full disappearance of intracranial U87-Luc glioblastoma in 100% of treated mice using magnetic hyperthermia.采用磁热疗,用聚赖氨酸包裹非致热磁小体矿化,导致 100%治疗组小鼠颅内 U87-Luc 神经胶质瘤完全消失。
Biomaterials. 2017 Oct;141:210-222. doi: 10.1016/j.biomaterials.2017.06.026. Epub 2017 Jun 21.
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The nitric oxide donor JS-K sensitizes U87 glioma cells to repetitive irradiation.一氧化氮供体JS-K使U87胶质瘤细胞对重复照射敏感。
Tumour Biol. 2017 Jun;39(6):1010428317703922. doi: 10.1177/1010428317703922.
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Nociceptin/orphanin FQ antagonizes lipopolysaccharide-stimulated proliferation, migration and inflammatory signaling in human glioblastoma U87 cells.孤啡肽受体拮抗剂抑制脂多糖刺激的人胶质母细胞瘤 U87 细胞增殖、迁移和炎症信号通路。
Biochem Pharmacol. 2017 Sep 15;140:89-104. doi: 10.1016/j.bcp.2017.05.021. Epub 2017 Jun 2.
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Mono-PEGylation of Alpha-MMC and MAP30 from Momordica charantia L.: Production, Identification and Anti-Tumor Activity.苦瓜中α-苦瓜素和MAP30的单聚乙二醇化:制备、鉴定及抗肿瘤活性
Molecules. 2016 Oct 31;21(11):1457. doi: 10.3390/molecules21111457.
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Origin of the U87MG glioma cell line: Good news and bad news.U87MG 神经胶质瘤细胞系的起源:好消息和坏消息。
Sci Transl Med. 2016 Aug 31;8(354):354re3. doi: 10.1126/scitranslmed.aaf6853.
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Evaluation of pseudoprogression rates and tumor progression patterns in a phase III trial of bevacizumab plus radiotherapy/temozolomide for newly diagnosed glioblastoma.贝伐单抗联合放疗/替莫唑胺治疗新诊断胶质母细胞瘤的III期试验中假性进展率和肿瘤进展模式的评估
Neuro Oncol. 2016 Oct;18(10):1434-41. doi: 10.1093/neuonc/now091. Epub 2016 Aug 11.
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Inhibitor of apoptosis protein expression in glioblastomas and their in vitro and in vivo targeting by SMAC mimetic GDC-0152.胶质母细胞瘤中凋亡抑制蛋白的表达及其被SMAC模拟物GDC-0152进行的体内外靶向作用
Cell Death Dis. 2016 Aug 4;7(8):e2325. doi: 10.1038/cddis.2016.214.
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Promise of bitter melon (Momordica charantia) bioactives in cancer prevention and therapy.苦瓜(Momordica charantia)生物活性物质在癌症预防和治疗中的前景。
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Akt and β-catenin contribute to TMZ resistance and EMT of MGMT negative malignant glioma cell line.Akt和β-连环蛋白促成MGMT阴性恶性胶质瘤细胞系的替莫唑胺耐药性和上皮-间质转化。
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MAP30通过抑制LGR5和Wnt/β-连环蛋白信号通路并增强Smac表达来促进U251和U87细胞的凋亡。

MAP30 promotes apoptosis of U251 and U87 cells by suppressing the LGR5 and Wnt/β-catenin signaling pathway, and enhancing Smac expression.

作者信息

Jiang Yilin, Miao Junjie, Wang Dongliang, Zhou Jingru, Liu Bo, Jiao Feng, Liang Jiangfeng, Wang Yangshuo, Fan Cungang, Zhang Qingjun

机构信息

Department of Neurosurgery, Peking University People's Hospital, Peking University, Beijing 100044, P.R. China.

Department of Neurosurgery, Peking University International Hospital, Beijing 102206, P.R. China.

出版信息

Oncol Lett. 2018 Apr;15(4):5833-5840. doi: 10.3892/ol.2018.8073. Epub 2018 Feb 16.

DOI:10.3892/ol.2018.8073
PMID:29556310
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5844066/
Abstract

Significant antitumor activity of anti-human immunodeficiency virus protein of 30 kDa (MAP30) purified from has been the subject of previous research. However, the effective mechanism of MAP30 on malignant glioma cells has not yet been clarified. The aim of the present study was to investigate the effects and mechanism of MAP30 on U87 and U251 cell lines. A Cell Counting Kit-8 assay, wound healing assay and Transwell assay were used to detect the effects on U87 and U251 cells treated with different concentrations of MAP30 (0.5, 1, 2, 4, 8 and 16 µM) over different periods of time. Proliferation, migration and invasion of each cell line were markedly inhibited by MAP30 in a dose- and time-dependent manner. Flow cytometry and fluorescence staining demonstrated that apoptosis increased and the cell cycle was arrested in S-phase in the two investigated cell lines following MAP30 treatment. Western blot analysis demonstrated that leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5) expression and key proteins in the Wnt/β-catenin signaling pathway were apparently decreased, whereas second mitochondria-derived activator of caspase (Smac) protein expression significantly increased with MAP30 treatment in the same manner. These results suggest that MAP30 markedly induces apoptosis in U87 and U251 cell lines by suppressing LGR5 and the Wnt/β-catenin signaling pathway, and enhancing Smac expression in a dose- and time-dependent manner.

摘要

从[具体来源]纯化的30 kDa抗人免疫缺陷病毒蛋白(MAP30)具有显著的抗肿瘤活性,这是先前研究的主题。然而,MAP30对恶性胶质瘤细胞的有效作用机制尚未阐明。本研究的目的是探讨MAP30对U87和U251细胞系的影响及其机制。采用细胞计数试剂盒-8法、伤口愈合试验和Transwell试验,检测不同浓度(0.5、1、2、4、8和16 μM)的MAP30在不同时间段处理U87和U251细胞后的效果。MAP30以剂量和时间依赖性方式显著抑制各细胞系的增殖、迁移和侵袭。流式细胞术和荧光染色表明,MAP30处理后,所研究的两种细胞系的凋亡增加,细胞周期停滞在S期。蛋白质印迹分析表明,富含亮氨酸重复序列的G蛋白偶联受体5(LGR5)的表达以及Wnt/β-连环蛋白信号通路中的关键蛋白明显降低,而第二线粒体衍生的半胱天冬酶激活剂(Smac)蛋白表达则以相同方式随MAP30处理显著增加。这些结果表明,MAP30通过抑制LGR5和Wnt/β-连环蛋白信号通路,并以剂量和时间依赖性方式增强Smac表达,从而显著诱导U87和U251细胞系凋亡。