一氧化氮对抗微管药物诱导的细胞凋亡的抑制作用：一种新的耐药机制的可能机制
Suppression of anti-microtubule agent-induced apoptosis by nitric oxide: possible mechanism of a new drug resistance.
作者信息
Ogura T, DeGeorge G, Tatemichi M, Esumi H
机构信息
Investigative Treatment Division, National Cancer Center Research Institute East, Kashiwa, Chiba.
出版信息
Jpn J Cancer Res. 1998 Feb;89(2):199-205. doi: 10.1111/j.1349-7006.1998.tb00549.x.
Abstract
The propensity of a cell to undergo apoptosis has been proposed to be a determinant of sensitivity to anti-microtubule agents. The anti-microtubule agents vincristine and paclitaxel induce key features of apoptosis, such as intranucleosomal DNA fragmentation and changes in nuclear morphology in the human neuroblastoma cell line, NB-39-nu. Nitric oxide (NO) generated from NO-releasing drugs prevented anti-microtubule agent-induced apoptosis in this cell line. The mechanism of suppression of apoptosis by NO appears to be via the inhibition of an interleukin-1beta converting enzyme-like protease cascade. This finding reveals a new biological function of NO, as well as a new molecular insight into resistance to chemotherapy with anti-microtubule agents.
摘要
细胞发生凋亡的倾向被认为是对抗微管药物敏感性的一个决定因素。抗微管药物长春新碱和紫杉醇可诱导人神经母细胞瘤细胞系NB-39-nu出现凋亡的关键特征，如核小体间DNA片段化和核形态改变。释放一氧化氮（NO）的药物所产生的NO可阻止该细胞系中抗微管药物诱导的凋亡。NO抑制凋亡的机制似乎是通过抑制白细胞介素-1β转化酶样蛋白酶级联反应。这一发现揭示了NO的一种新的生物学功能，以及对使用抗微管药物进行化疗耐药性的新分子见解。
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本文引用的文献
1
Nitric oxide inhibits CPP32-like activity under redox regulation.一氧化氮在氧化还原调节下抑制类CPP32活性。
Biochem Biophys Res Commun. 1997 Jul 18;236(2):365-9. doi: 10.1006/bbrc.1997.6948.
2
Suppression of apoptosis by nitric oxide via inhibition of interleukin-1beta-converting enzyme (ICE)-like and cysteine protease protein (CPP)-32-like proteases.一氧化氮通过抑制白细胞介素-1β转化酶（ICE）样和半胱氨酸蛋白酶蛋白（CPP）-32样蛋白酶来抑制细胞凋亡。
J Exp Med. 1997 Feb 17;185(4):601-7. doi: 10.1084/jem.185.4.601.
3
The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosis.细胞色素c从线粒体的释放：Bcl-2调控细胞凋亡的主要位点。
Science. 1997 Feb 21;275(5303):1132-6. doi: 10.1126/science.275.5303.1132.
4
Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked.Bcl-2对细胞凋亡的预防作用：线粒体中细胞色素c的释放受阻。
Science. 1997 Feb 21;275(5303):1129-32. doi: 10.1126/science.275.5303.1129.
5
Apoptosis as a mechanism of cell death induced by different chemotherapeutic drugs in human leukemic T-lymphocytes.
Biochem Pharmacol. 1996 May 17;51(10):1331-40. doi: 10.1016/0006-2952(96)00041-x.
6
Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c.无细胞提取物中凋亡程序的诱导：对dATP和细胞色素c的需求
Cell. 1996 Jul 12;86(1):147-57. doi: 10.1016/s0092-8674(00)80085-9.
7
A license to kill.杀人执照。
Cell. 1996 Jun 14;85(6):781-4. doi: 10.1016/s0092-8674(00)81005-3.
8
Resistance to apoptotic cell death in a drug resistant T cell leukaemia cell line.耐药性T细胞白血病细胞系对凋亡性细胞死亡的抗性
Leukemia. 1996 Mar;10(3):447-55.
9
Paclitaxel-induced apoptosis in human gastric carcinoma cell lines.紫杉醇诱导人胃癌细胞系凋亡
Cancer. 1996 Jan 1;77(1):14-8. doi: 10.1002/(SICI)1097-0142(19960101)77:1<14::AID-CNCR4>3.0.CO;2-N.
10
Sequential activation of ICE-like and CPP32-like proteases during Fas-mediated apoptosis.Fas介导的细胞凋亡过程中ICE样和CPP32样蛋白酶的顺序激活。
Nature. 1996 Apr 25;380(6576):723-6. doi: 10.1038/380723a0.
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