摘要
目的:探讨三氧化二砷(As2O3)抑制鼻咽癌的作用机制。方法:采用流式细胞仪(FCM)、激光扫描共聚焦显微镜(LSCM)和荧光技术,检测人鼻咽癌细胞株(CNE1)经As2O3诱导后细胞连接蛋白43(Cx43)表达的变化。结果:FCM显示,经过浓度为4μmol L的As2O3处理后,其Cx43阳性细胞计数率明显升高,与未经As2O3处理和经2μmol L的As2O3处理的CNE1比较,其差异具有非常显著性意义(p<0.01);LSCM图像观察到,经4μmol LAs2O3处理后,标记Cx43的绿色荧光显著增强,集中分布于细胞膜。结论:较高剂量浓度的As2O3能提高鼻咽癌细胞Cx43的表达率,升高细胞膜Cx43的含量。As2O3抑制鼻咽癌细胞生长的作用机制之一,是通过恢复细胞间隙连接通讯功能来实现的。
Objective: To study the mechanisms of arsenic trioxide (As_2O_3) against nasopharyngeal carcinoma. Methods: The variation of Cx43 expression in human nasopharyngeal carcinoma cell lines(CNE1)were observed under the flow cytometry, the laser scanning confocal microscopy and technology of fluorescence.Results: The positive rates of Cx43 in CNE1 that treated with 4umol/L As_2O_3 was significantly higher than that either treated with 2 μmol/L As_2O_3 or untreated with As_2O_3 (P <0.01). The scanning images displayed that the fluorescence signal of Cx43 in cell membrane of CNE1 that treated with 4 μmol/L As_2O_3 was significantly strengthened than that untreated with As_2O_3. Conclusions: The higher concentration of As_2O_3 can increase the expression of Cx43 in CNE1 and increase the content of Cx43 in cell membrane of CNE1. One of its mechanisms against nasopharyngeal carcinoma is to renew the gap junctional intercellular communication.
出处
《激光生物学报》
CAS
CSCD
2004年第6期443-446,共4页
Acta Laser Biology Sinica
基金
广东省医学科学技术研究基金资助项目(A2003501)
关键词
三氧化二砷
鼻咽肿瘤
连接蛋白43
流式细胞仪
激光共聚焦显微镜
arsenic trioxide (As_2O_3)
carcinoma
nasopharyngeal neoplasm
connexin 43
flow cytometry
laser scanning confocal microscopy
