%0 Journal Article
%T 全反式维甲酸联合5？卜？尿嘧啶对Eca109细胞增殖、迁移和VEGF表达的影响*<br>Effects of all？？trans retinoic acid combined with 5？？fluorouracil on proliferation, migration, and VEGF expression of Eca109 cells
%A 李珊珊
%A 罗忠民
%A 崔会娟
%A 王珍珍
%A 彭湃
%A 李娜
%A 路太英
%J 郑州大学学报（医学版）
%D 2015
%X 摘要目的：探讨全反式维甲酸(ATRA)、5？卜？尿嘧啶(5？？FU)单独或联合作用对Eca109细胞增殖、迁移和血管内皮生长因子(VEGF)表达的影响。 方法：将常规传代的Eca109细胞分为4组：ATRA组、5？？FU组、ATRA+5？？FU组和对照组，采用MTT法检测各组细胞的增殖情况，通过划痕实验测定各组细胞的迁移能力，采用RT？？PCR和免疫细胞化学法分别检测各组细胞VEGF mRNA和蛋白的表达情况。 结果：作用24、48和72 h后，ATRA+5？？FU组的细胞生长抑制率均高于其他2组(F=23.432、13.605、73.369，P均<0.05）；作用24 h后，ATRA+5？？FU组的迁移率均低于其他3组（P均＜0.001）;作用48 h后，ATRA+5？？FU组细胞VEGF mRNA和蛋白的相对表达量均低于其他3组(P均<0.05)。 结论：ATRA、5？？FU均能抑制食管癌细胞的增殖，且联合用药效果更为显著，可能与其抑制肿瘤血管生成有关。<br>Abstract Aim: To discuss effects of all？？trans retinoic acid (ATRA), 5？？fluorouracil (5？？FU) alone or combined on proliferation, migration and VEGF expression of Eca109 cells. Methods: The cultured Eca109 cells were randomly divided into four groups: ATRA group, 5？？FU group, ATRA plus 5？？FU group, and control group. The cell growth inhibition rate of Eca109 cells was detected by MTT assay. Wound healing assay was used to observe the mobility rate. The mRNA and protein expressions of VEGF in the cells were detected by RT？？PCR and SABC method. Results: The cell growth inhibition rate of ATRA plus 5？？FU group was higher than those of the other two groups at 24，48 and 72 h after treatment(F=23.432, 13.605, 73.369, P<0.05). The mobility rate of ATRA plus 5？？FU group was lower than those of the other three groups at 24 h after treament(P＜0.001). The relative expressions of VEGF mRNA and protein of ATRA plus 5？？FU group was lower than those of the other three groups(P<0.05). Conclusion: ATRA and 5？？FU could inhibit the proliferation of Eca109 cells. ATRA combined with 5？？FU shows a synergistic effect on suppressing the proliferation of Eca109 cells, which may be related to its inhibition of tumor angiogenesis
%K 全反式维甲酸
%K 5？卜？尿嘧啶
%K Eca109细胞
%K 肿瘤血管生成
%K 血管内皮生长因子&lt
%K br&gt
%K esophageal squamous cell carcinoma
%K EC？？1 cell
%K pXJ40？？Stat3
%K p？？Stat3 protein
%K transfection
%U http://jms.zzu.edu.cn/oa/darticle.aspx?type=view&id=201501001