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鼻咽癌细胞CIC-3在细胞周期中的表达(英文)
引用本文:王立伟,陈丽新,Tim JACOB. 鼻咽癌细胞CIC-3在细胞周期中的表达(英文)[J]. 生理学报, 2004, 0(2)
作者姓名:王立伟  陈丽新  Tim JACOB
作者单位:广东医学院生理学教研室、细胞生物学研究室,广东医学院生理学教研室、细胞生物学研究室,加的夫大学生物科学学院 广东湛江 524023,广东湛江 524023,加的夫CF10 3US,英国
基金项目:This work was supported by grants from the Wellcome Trust UK (056909/299/Z),the Education Ministry of China (GJ9901) and the Health Department of Guangdong Province (A2001474).
摘    要:用免疫荧光、激光共聚焦显微镜图像分析及膜片钳等技术研究了鼻咽癌上皮cNE-2Z细胞容积激活性氯通道候选基因C1C-3的表达及其在细胞周期中与容积激活性氯电流及细胞容积调节性回缩(regulatorly volume decrease,RVD)的关系。结果显示,CNE-2Z细胞表达CIC-3。C1C-3蛋白主要位于细胞内而不是在细胞膜上,其表达水平及其在细胞中的分布呈细胞周期依赖性。G1期细胞的C1C-3表达水平较低而S期则较高,M期细胞的表达水平中等。在细胞周期中,C1C-3表达水平与细胞RVD能力及容积激活性氯电流水平呈反比。上述观察结果提示,C1C-3可能参与细胞周期的调节,但CNE-2Z细胞中的C1C-3可能不是与RVD有关的氯通道。

关 键 词:肿瘤细胞  CIC-3蛋白  氯通道  基因表达  细胞周期

C1C-3 expression in the cell cycle of nasopharyngeal carcinoma cells
WANG Li-Wei,CHEN Li-Xin,Tim JACOB. C1C-3 expression in the cell cycle of nasopharyngeal carcinoma cells[J]. Acta Physiologica Sinica, 2004, 0(2)
Authors:WANG Li-Wei  CHEN Li-Xin  Tim JACOB
Affiliation:WANG Li-Wei,CHEN Li-Xin,Tim JACOBDepartment of Physiology and Laboratory of Cell Biology,Guangdong Medical College,Zhanjiang,Guangdong 524023,China School of Biosciences,Cardiff University,Cardiff CF10 3US,UK.
Abstract:The immunofluorescence approach, the confocal microscopy and the patch-clamp technique were used to investigate the expression of C1C-3 (one of the candidates of volume-activated chloride channels) and its relationships with the volume-activated chloride current and the capacity of regulatory volume decrease (RVD) in the cell cycle of nasopharyngeal carcinoma cells (CNE-2Z cells). The results indicated that CNE-2Z cells expressed C1C-3. C1C-3 was located predominantly inside the cells but not in the membrane. Both the expression level and the distribution of C1C-3 were cell cycle dependent. C1C-3 expression was low in Gl but high in S phase. The cells in G2/M phase possessed an intermediate level of the expression. C1C-3 expression level was negatively correlated to the RVD capacity and amplitude of the volume-activated chloride current in the cell cycle. The results suggest that C1C-3 may be an important factor in the regulation of cell cycle progression, but that it is probably not the chloride channel associated with RVD in these cancer cells.
Keywords:tumour cells  C1C-3 protien  chloride channels  gene expression  cell cycle
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