天津医药

天津医药 ›› 2020, Vol. 48 ›› Issue (5): 353-357.doi: 10.11958/20182226

• 细胞与分子生物学 •    下一篇

褪黑素增强紫杉醇对膀胱癌 T24细胞增殖的抑制作用 #br#

陈欢 1，朱佳斌 2，赵晓瑾 2，董传江 1△，董自强 1△
  

  1. 1湖北省宜昌市，三峡大学第一临床医学院泌尿外科（邮编 443000）；2三峡大学附属仁和医院神经外科

  • 收稿日期:2019-01-03 修回日期:2019-06-19 出版日期:2020-05-15 发布日期:2020-06-24
  • 作者简介:陈欢（1991），男，硕士研究生，住院医师，主要从事泌尿外科肿瘤防治方面研究
  • 基金资助:
    国家自然科学基金资助项目（81300626）

Melatonin enhances the inhibitory effect of paclitaxel on T24 cell proliferation #br#

CHEN Huan1, ZHU Jia-bin2, ZHAO Xiao-jin2, DONG Chuan-jiang1,2△, DONG Zi-qiang1△ #br#   

  1. 1 Department of Urology, the First College of Clinical Medical Science of Three Gorges University, Yichang 443000, China;
    2 Department of Neurosurgery, the Affiliated Renhe Hospital of China Three Gorges University
  • Received:2019-01-03 Revised:2019-06-19 Published:2020-05-15 Online:2020-06-24

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摘要：

摘要：目的 观察褪黑素（melatonin，Mel）与紫杉醇（paclitaxel，PTX）协同对膀胱癌 T24细胞的抑制作用，并探讨
其作用机制。方法 Mel和化疗药物 PTX单独使用或者联合使用处理 T24细胞，用 CCK-8法和平板克隆形成实验检
测 Mel和 PTX对 T24细胞的增殖抑制作用及半数抑制浓度（IC50）；RT-PCR和 Western-blot检测 T24细胞中环氧化物
酶-2（COX-2）的 mRNA和蛋白水平；采用双荧光素酶报告基因检测 NF-kB的启动子区活性。结果 与单独 PTX组
相比，Mel能够显著增强 PTX对 T24细胞增殖的抑制作用并降低 PTX的 IC50值，T24细胞的增殖能力、克隆形成能力显
著下降（P＜0.05）；联合用药可以显著降低 COX-2的 mRNA和蛋白水平及其相关信号通路核转录因子（NF）-kB的启
动子活性。结论 Mel与 PTX可协同抑制 T24膀胱癌细胞的增殖，其机制可能与抑制 NF-kB信号通路启动子活性，
从而降低 T24细胞内 COX-2的表达有关。

关键词: 褪黑激素, 紫杉酚, 膀胱肿瘤, 环氧化酶 2, NF-κB

Abstract:

Abstract: Objective To observe the inhibitory effect of melatonin (Mel) and paclitaxel (PTX) on T24 bladder cancer
cells and to explore the underlying mechanism. Methods T24 cells were treated with Mel and PTX alone or in
combination. CCK-8 assay and plate colony formation assay were used to detect the proliferation inhibition or IC50 value of
Mel and PTX on T24 cells. The mRNA and protein levels of COX-2 in T24 cells were detected by RT-PCR and Western
blot assays. The promoter activity of NF-kB was detected by dual-luciferase reporter assay. Results Compared with the
PTX treatment alone, Mel can significantly enhance the inhibitory effect of PTX on T24 cell proliferation and decrease the
IC
50 value of PTX. The proliferation and colony formation ability of T24 cells were decreased significantly (P＜0.05).
Combination therapy with Mel and PTX could significantly reduce the protein and mRNA level of COX-2 and the promoter
activity of its related NF-kB signaling pathway. Conclusion Mel and PTX could synergistically inhibit the proliferation of
T24 bladder cancer cells, which may be related to the inhibition of NF-kB signaling pathway promoter activity and the
decrease of COX-2 expression in T24 cells.

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