生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2004年
2期
230-236
,共7页
王立伟%陈丽新%Tim JACOB
王立偉%陳麗新%Tim JACOB
왕립위%진려신%Tim JACOB
肿瘤细胞%ClC-3蛋白%氯通道%基因表达%细胞周期
腫瘤細胞%ClC-3蛋白%氯通道%基因錶達%細胞週期
종류세포%ClC-3단백%록통도%기인표체%세포주기
tumour cells%ClC-3 protien%chloride channels%gene expression%cell cycle
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(regulatoryvolumedecrease,RVD)的关系.结果显示,CNE-2Z细胞表达ClC-3.ClC-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ClC-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,ClC-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,ClC-3可能参与细胞周期的调节,但CNE-2Z细胞中的ClC-3可能不是与RVD有关的氯通道.
用免疫熒光、激光共聚焦顯微鏡圖像分析及膜片鉗等技術研究瞭鼻嚥癌上皮CNE-2Z細胞容積激活性氯通道候選基因C1C-3的錶達及其在細胞週期中與容積激活性氯電流及細胞容積調節性迴縮(regulatoryvolumedecrease,RVD)的關繫.結果顯示,CNE-2Z細胞錶達ClC-3.ClC-3蛋白主要位于細胞內而不是在細胞膜上,其錶達水平及其在細胞中的分佈呈細胞週期依賴性.G1期細胞的ClC-3錶達水平較低而S期則較高,M期細胞的錶達水平中等.在細胞週期中,ClC-3錶達水平與細胞RVD能力及容積激活性氯電流水平呈反比.上述觀察結果提示,ClC-3可能參與細胞週期的調節,但CNE-2Z細胞中的ClC-3可能不是與RVD有關的氯通道.
용면역형광、격광공취초현미경도상분석급막편겸등기술연구료비인암상피CNE-2Z세포용적격활성록통도후선기인C1C-3적표체급기재세포주기중여용적격활성록전류급세포용적조절성회축(regulatoryvolumedecrease,RVD)적관계.결과현시,CNE-2Z세포표체ClC-3.ClC-3단백주요위우세포내이불시재세포막상,기표체수평급기재세포중적분포정세포주기의뢰성.G1기세포적ClC-3표체수평교저이S기칙교고,M기세포적표체수평중등.재세포주기중,ClC-3표체수평여세포RVD능력급용적격활성록전류수평정반비.상술관찰결과제시,ClC-3가능삼여세포주기적조절,단CNE-2Z세포중적ClC-3가능불시여RVD유관적록통도.
The immunofluorescence approach, the confocal microscopy and the patch-clamp technique were used to investigate the expression of ClC-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 ClC-3. ClC-3 was located predominantly inside the cells but not in the membrane. Both the expression level and the distribution of ClC-3 were cell cycle dependent. ClC-3 expression was low in G1 but high in S phase. The cells in G2/M phase possessed an intermediate level of the expression. ClC-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.