张玉军, 齐凤英, 刘淑霞, 左连富, 郭建文, 刘江惠. 戊地昔布对人食管癌Eca109细胞系的抑制作用及其调控[J]. 中国肿瘤临床, 2005, 32(9): 508-512.
引用本文: 张玉军, 齐凤英, 刘淑霞, 左连富, 郭建文, 刘江惠. 戊地昔布对人食管癌Eca109细胞系的抑制作用及其调控[J]. 中国肿瘤临床, 2005, 32(9): 508-512.
Zhang Yujun, Qi Fengying, Liu Shuxia, Zuo Lianfu, Guo Jianwen, Liu Jianghui. The Inhibition of Valdecoxib on the Proliferation of Human Esophageal Cancer Cells[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2005, 32(9): 508-512.
Citation: Zhang Yujun, Qi Fengying, Liu Shuxia, Zuo Lianfu, Guo Jianwen, Liu Jianghui. The Inhibition of Valdecoxib on the Proliferation of Human Esophageal Cancer Cells[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2005, 32(9): 508-512.

戊地昔布对人食管癌Eca109细胞系的抑制作用及其调控

The Inhibition of Valdecoxib on the Proliferation of Human Esophageal Cancer Cells

  • 摘要: 目的: 探讨特异选择性环氧化酶-2(COX-2)抑制剂戊地昔布对人食管癌Eca109细胞的抑制作用及其调控机制. 方法: 采用MTT法检测戊地昔布对人食管癌Eca109细胞生长的作用;流式细胞术检测细胞凋亡和细胞周期分布;采用流式细胞术和免疫组织化学检测人食管癌Eca109细胞中p-p38MAPK、c-jun和c-fos的表达. 结果: 戊地昔布(25~400μmol/L)可按时间和浓度依赖性抑制人食管癌Eca109细胞的生长,作用72小时后,对细胞生长的抑制率可达85.95%,凋亡率由(2.38±0.42)%增加到(48.46±0.73)%;50~400μmol/L时增殖指数和S期的细胞比例则明显降低,G0/G1期的细胞比例增加.戊地昔布在给药72小时后,食管癌Eca109细胞中p-p38MAPK、c-fos、c-jun蛋白表达均增强,并且随浓度的增加而增强. 结论: 戊地昔布可通过诱导细胞凋亡和细胞周期停滞而抑制人Eca109细胞生长,其诱导凋亡的机制可能部分是通过激活p-p38MAPK、c-jun、c-fos途径实现的.

     

    Abstract: Objective :To study the effect and mechanism of valdecoxib, a selective COX-2in-hibitor, on human esophageal Eca109 cell line. Methods :MTT assay and flow cytometry were used to observe the effect of valdecoxib on proliferation, apoptosis and the cell cycle distribution of Eca109 cells. The expression of p-p38, c-fos or c-jun protein was detected by flow cytometry and immunocytochemical staining. Results :Valdecoxib in 25400 (mo1.Lsignificantly inhibited the proliferation of Eca109 cell line in a time-and dose Iependent fashion, the inhibition rate of proliferation was 23.09 85.95% after 72h, and the rate of apoptosis was increased from (2.38±0.42)% to (2.95±o.8s)%-(48.46±0.73)%, 50400(mo1.L-1 valdecoxib also decreased the proliferation index and the proportion of cells in the S phase, increased the proportion of cells in the Go/G, phase, but had no effect on the proportion of cells in the GZ/M phase. Immunoc ytochemically, the positive stainings for p-p38, c-fos and c-jun were almost observed in nucleus of the Eca109 cells. Compared with those in Eca109 cells cultured in the medium with solvent, the stainings were strengthened for p-p38, c-fos and c-jun in the Eca109 cells exposed to valdecoxib in a dose lependent in 72h. Conclusions :Valdecoxib inhibits the growth of human esophageal Eca109 cell line by inducing apoptosis and cell cycle arrest. The mechanism of inducing apoptosis is partly realized by activating the p-p38/c-fos, c-jun.

     

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