三氧化二砷抑制食管癌细胞侵袭能力的机制研究

Molecular mechanism of As2 O3 in suppressing metastasis of esophagus carcinoma cells

目的：观察三氧化二砷（ As2 O3）对食管癌细胞侵袭能力的影响并探讨其分子机制。方法食管癌细胞经As2 O3处理后，MTT比色法检测细胞增殖能力，细胞黏附实验与侵袭实验检测细胞转移能力，Western blot检测转移相关蛋白金属基质蛋白酶（MMP）2、MMP9、E-cadherin及O型受体蛋白酪氨酸磷酸酶（PTPRO）表达水平。结果不同浓度As2O3处理显著抑制EC9706与EC109细胞增殖与侵袭能力，同未加药（0μmol/L）的对照组比较差异均有统计学意义（ P ＜0.01）；As2 O3处理可以减弱MMP2与MMP9的表达水平（ P ＜0.01），增强E-cadherin 与PTPRO的表达水平（ P ＜0.01）。结论As2 O3对食管癌细胞的恶性转移能力有显著的抑制作用，下调MMP2与MMP9的表达、同时上调E-cadherin与PTPRO的表达，可能是其抑制转移的分子机制。

Objective To investigate the molecular mechanism of As 2 O3 in suppressing metastasis of esophagus carcinoma cells.Methods The 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyl-tetrazolium bromide （MTT） assay, adhesion and invasion assay were performed to observe the inhibitory effect of As 2 O3 on proliferation and metastasis of esophagus carcinoma cells .The expressions of matrix metalloproteinases （ MMP）2, MMP9, E-cadherin, and protein tyrosine phosphatase receptor-type O （ PTPRO） were analyzed with Western blot .Results Exposure to As 2 O3 significantly presented suppressive functions on growth and metastasis of esophagus carcinoma cells in a dose-dependent manner （ P ＆lt;0.01 ） .Additionally , MMP2 and MMP9 expressions were increased after treatment with casticin （ P ＆lt;0.01 ） , whereas E-cadherin and PTPRO expressions were down-regulated （ P ＆lt;0.01 ） .Conclusions As2 O3 had a significant function to inhibit proliferation and metastasis of esophagus carcinoma cells .