Suppression of anti-microtubule agent-induced apoptosis by nitric oxide: Possible mechanism of a new drug resistance
Suppression of anti-microtubule agent-induced apoptosis by nitric oxide: Possible mechanism of a new drug resistance
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DOI：
10.1111/j.1349-7006.1998.tb00549.x
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发表时间：
1998-02-01
期刊：
影响因子：
--
通讯作者：
Esumi, H
中科院分区：
文献类型：
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作者：
Ogura, T;DeGeorge, G;Esumi, H
细胞发生凋亡的倾向已被认为是抗微管药物敏感性的决定因素。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的关键凋亡特征，如核内体DNA断裂和核形态变化。一氧化氮释放药物产生的一氧化氮（NO）可阻止抗微管药物诱导的细胞凋亡。NO抑制细胞凋亡的机制似乎是通过抑制白细胞介素-1 β转换酶样蛋白酶级联反应。这一发现揭示了NO的新的生物学功能，以及抗微管药物化疗耐药的新分子见解。
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-1 beta 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.