The ClC-3 chloride channel associated with microtubules is a target of paclitaxel in its induced-apoptosis.
The ClC-3 chloride channel associated with microtubules is a target of paclitaxel in its induced-apoptosis.
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与微管相关的 ClC-3 氯离子通道是紫杉醇诱导细胞凋亡的靶点
DOI：
10.1038/srep02615
复制
发表时间：
2013
影响因子：
4.6
通讯作者：
Chen, Lixin
中科院分区：
文献类型：
--
作者：
Zhang, Haifeng;Li, Huarong;Yang, Lili;Deng, Zhiqin;Luo, Hai;Ye, Dong;Bai, Zhiquan;Zhu, Linyan;Ye, Wencai;Wang, Liwei;Chen, Lixin
最近的证据表明，阳离子通量在细胞凋亡中起着关键作用。本研究探讨了氯−通道在紫杉醇诱导鼻咽癌CNE-2Z细胞凋亡中的作用。用紫杉醇诱导氯电流，用氯通道阻断剂抑制细胞凋亡。紫杉醇激活电流具有与体积激活氯电流相似的特性。ClC-3-siRNA下调ClC-3后，低张激活的氯电流和紫杉醇诱导的氯电流明显减少，提示参与紫杉醇诱导细胞凋亡的氯通道可能是ClC-3。在早期凋亡的细胞中，ClC-3显著上调；ClC-3过度表达聚集在细胞膜上形成交叉丝，并与α-微管蛋白共定位；原子力显微镜观察细胞膜超微结构的变化和柔韧性的降低。提示ClC-3是紫杉醇的重要靶点，ClC-3参与细胞凋亡可能与其膜微管堆积和过度激活有关。
Recent evidences show that cationic fluxes play a pivotal role in cell apoptosis. In this study, the roles of Cl− channels in paclitaxel-induced apoptosis were investigated in nasopharyngeal carcinoma CNE-2Z cells. Chloride current and apoptosis were induced by paclitaxel and inhibited by chloride channel blockers. Paclitaxel-activated current possessed similar properties to volume-activated chloride current. After ClC-3 was knocked-down by ClC-3-siRNA, hypotonicity-activated and paclitaxel-induced chloride currents were obviously decreased, indicating that the chloride channel involved in paclitaxel-induced apoptosis may be ClC-3. In early apoptotic cells, ClC-3 was up-regulated significantly; over-expressed ClC-3 was accumulated in cell membrane to form intercrossed filaments, which were co-localized with α-tubulins; changes of ultrastructures and decrease of flexibility in cell membrane were detected by atomic force microscopy. These suggest that ClC-3 is a critical target of paclitaxel and the involvement of ClC-3 in apoptosis may be associated with its accumulation with membrane microtubules and its over activation.
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发表时间：
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影响因子：
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作者：
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