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[三氧化二砷与青蒿素抗癌机制的研究进展]

[Research progress on anti-cancer mechanisms of arsenic trioxide and artemisinin].

作者信息

Yue Qing-xi, Yu Hong, He Ting, Yu Hai-qing

出版信息

Yao Xue Xue Bao. 2016 Feb;51(2):208-14.

PMID:29856573
Abstract

The formation and metastasis of tumor cells are closely related to the gene regulation. It is critical to elucidate the molecular mechanism of a compound using in cancer therapy. In this article, we reviewed the anti-cancer molecular mechanism of arsenic trioxide and artemisinin. Its anti-cancer function mainly includes: regulation of cell cycle regulatory proteins to inhibit tumor cell proliferation, cell apoptosis signal transduction pathway to promote apoptosis in tumor cells, immortalization associated genes to reduce the life of tumor cells, angiogenesis/invasion/metastasis gene to block the spread of tumor cells, promoter methylation and protein ubiquitination gene to enhance anti-oncogene expression and ubiquitin- mediated protein degradation, micro RNA to inhibit proliferation or induce apoptosis in tumor cells, DNA synthesis and repair of DNA damage and repair gene to decrease the DNA synthesis of tumor cells, signal transduction pathways of cell proliferation/apoptosis and invasion/metastasis etc., the expression of hormone receptors and so on. We indicated the problems existing in current studies and also prospected the future of using the compound to fight cancer.

摘要

肿瘤细胞的形成和转移与基因调控密切相关。阐明一种用于癌症治疗的化合物的分子机制至关重要。在本文中,我们综述了三氧化二砷和青蒿素的抗癌分子机制。其抗癌功能主要包括:调节细胞周期调节蛋白以抑制肿瘤细胞增殖、细胞凋亡信号转导通路以促进肿瘤细胞凋亡、永生化相关基因以缩短肿瘤细胞寿命、血管生成/侵袭/转移基因以阻止肿瘤细胞扩散、启动子甲基化和蛋白质泛素化基因以增强抗癌基因表达和泛素介导的蛋白质降解、微小RNA以抑制肿瘤细胞增殖或诱导其凋亡、DNA合成以及DNA损伤修复基因以减少肿瘤细胞的DNA合成、细胞增殖/凋亡以及侵袭/转移等信号转导通路、激素受体的表达等。我们指出了当前研究中存在的问题,并对使用该化合物抗癌的未来进行了展望。

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1
[Research progress on anti-cancer mechanisms of arsenic trioxide and artemisinin].[三氧化二砷与青蒿素抗癌机制的研究进展]
Yao Xue Xue Bao. 2016 Feb;51(2):208-14.
2
Arsenic trioxide inhibits CXCR4-mediated metastasis by interfering miR-520h/PP2A/NF-κB signaling in cervical cancer.三氧化二砷通过干扰宫颈癌中miR-520h/PP2A/NF-κB信号通路抑制CXCR4介导的转移。
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microRNA expression alteration after arsenic trioxide treatment in HepG-2 cells.三氧化二砷处理 HepG-2 细胞后 microRNA 表达的改变。
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Artesunate possesses anti-leukemia properties that can be enhanced by arsenic trioxide.青蒿琥酯具有抗白血病特性,三氧化二砷可增强其抗白血病特性。
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Arsenic trioxide induces apoptosis in pancreatic cancer cells via changes in cell cycle, caspase activation, and GADD expression.三氧化二砷通过细胞周期变化、半胱天冬酶激活及生长停滞和DNA损伤诱导基因(GADD)表达改变,诱导胰腺癌细胞凋亡。
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Arsenic trioxide causes redistribution of cell cycle, caspase activation, and GADD expression in human colonic, breast, and pancreatic cancer cells.三氧化二砷可导致人结肠癌细胞、乳腺癌细胞和胰腺癌细胞的细胞周期重新分布、半胱天冬酶激活以及生长停滞和DNA损伤诱导基因表达。
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Arsenic trioxide inhibits Hedgehog, Notch and stem cell properties in glioblastoma neurospheres.三氧化二砷抑制神经胶质瘤球体中的 Hedgehog、Notch 和干细胞特性。
Acta Neuropathol Commun. 2014 Mar 31;2:31. doi: 10.1186/2051-5960-2-31.
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Arsenic Trioxide Inhibits Cell Growth and Invasion via Down- Regulation of Skp2 in Pancreatic Cancer Cells.三氧化二砷通过下调Skp2抑制胰腺癌细胞的生长和侵袭。
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TG-interacting factor transcriptionally induced by AKT/FOXO3A is a negative regulator that antagonizes arsenic trioxide-induced cancer cell apoptosis.由AKT/FOXO3A转录诱导的TG相互作用因子是一种负调节因子,可拮抗三氧化二砷诱导的癌细胞凋亡。
Toxicol Appl Pharmacol. 2015 May 15;285(1):41-50. doi: 10.1016/j.taap.2015.03.007. Epub 2015 Mar 16.
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Arsenic trioxide reduces the invasive and metastatic properties of nasopharyngeal carcinoma cells in vitro.三氧化二砷在体外降低鼻咽癌细胞的侵袭和转移特性。
Braz J Med Biol Res. 2006 May;39(5):677-85. doi: 10.1590/s0100-879x2006000500015. Epub 2006 Apr 20.