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三氧化二砷抑制人鼻咽癌细胞侵袭的体外实验研究[J]. 肿瘤防治研究, 2005, 32(03): 129-131. DOI: 10.3971/j.issn.1000-8578.637
引用本文: 三氧化二砷抑制人鼻咽癌细胞侵袭的体外实验研究[J]. 肿瘤防治研究, 2005, 32(03): 129-131. DOI: 10.3971/j.issn.1000-8578.637
Effect of Arsenic Trioxide on Invasion of Human Nasopharyngeal Carcinoma Cells in Vitro[J]. Cancer Research on Prevention and Treatment, 2005, 32(03): 129-131. DOI: 10.3971/j.issn.1000-8578.637
Citation: Effect of Arsenic Trioxide on Invasion of Human Nasopharyngeal Carcinoma Cells in Vitro[J]. Cancer Research on Prevention and Treatment, 2005, 32(03): 129-131. DOI: 10.3971/j.issn.1000-8578.637

三氧化二砷抑制人鼻咽癌细胞侵袭的体外实验研究

Effect of Arsenic Trioxide on Invasion of Human Nasopharyngeal Carcinoma Cells in Vitro

  • 摘要: 目的 观察三氧化二砷(As2O3)对人鼻咽癌细胞株HNEl-LMPl侵袭、转移的影响。方法 鼻咽癌细胞在含3μmol/L的As2O3培养基中培养48小时。然后在无含砷的培养基中继续培养48小时后,收集此时间点贴壁的细胞作为研究对象;用细胞-基质黏附实验、细胞运动实验和肿瘤细胞重组基底膜侵袭实验检测As2O3对HNEl-LMPl细胞黏附、运动及侵袭能力的影响;用激光共聚焦的方法检测EB病毒编码的潜伏膜蛋白1(LMPl)的表达情况。结果 肿瘤细胞-基质黏附实验结果显示,经As2O3处理的HNEl-LMPl细胞,其黏附能力(平均吸光度为0.524±0.09)低于对照组细胞(平均吸光度为0.665±0.14),两者相比有差异(P<0.05)。运动实验和肿瘤细胞重组基底膜侵袭结果均显示,经As2O3处理后,穿过游离的聚乙烯吡咯烷酮膜(PVP-F)的肿瘤细胞数明显减少(P<0.01),同时As2O3能够下调LMPl的表达。结论As2O3具有抗人鼻咽癌细胞株转移的潜力,其机制可能与抑制LMPl的表达相关。

     

    Abstract: Abstract :Objective  The study was designed to investigate the effect of arsenic t rioxide (As2O3 ) on metastasis of nasopharyngeal carcinoma cell line HNE1-LMP1. Methods  HNE1-LMP1 cells were cultured in the media containing 3μmol/ L of As2O3 for 48 hours and then recovered in the free drug media for following 48 hours. Af terwards, only the attached cells were collected to analyze its metastasis potential. Reconstituted basement membrane invasive assay was used to evaluate the ability of adhesion, migration and invasion in HNE1-LMP1 cells. Confocal microscopy was performed to observe the expression of latent membrane protein 1 (LMP1) . Results  As2O3 significantly inhibited membrane adhesion and invasion as well as migration of HNE1-LMP1 cells. The expression of LMP1 was also reduced as demonst rated by Confocal microscopy examination. Conclusion  As2O3 was a potential agent inhibiting NPC invasion and metastasis. The mechanism might be associated with the reduction of LMP1 expression.

     

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