FoxM1 down-regulation promotes sensitivity of laryngeal carcinoma Hep-2 cells to cisplatin

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FoxM1 down-regulation promotes sensitivity of laryngeal carcinoma Hep-2 cells to cisplatin

更新时间：2026-01-09

- FoxM1 down-regulation promotes sensitivity of laryngeal carcinoma Hep-2 cells to cisplatin
- Journal of Army Medical University Vol. 37, Issue 16, Pages: 1603-1608(2015)
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  CLC： R73-361;R739.65;R979.19
- Published：2015
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魏蕾,江黎珠,于超,文韬宇,陈鸿雁.下调FoxM1表达对人喉癌Hep-2细胞顺铂敏感性的影响[J].陆军军医大学学报(原第三军医大学学报),2015,37(16):1603-1608.

　Wei Lei,Jiang Lizhu,Yu Chao,Wen Taoyu,Chen Hongyan.FoxM1 down-regulation promotes sensitivity of laryngeal carcinoma Hep-2 cells to cisplatin[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(16):1603-1608.
魏蕾,江黎珠,于超,文韬宇,陈鸿雁.下调FoxM1表达对人喉癌Hep-2细胞顺铂敏感性的影响[J].陆军军医大学学报(原第三军医大学学报),2015,37(16):1603-1608. DOI：

　Wei Lei,Jiang Lizhu,Yu Chao,Wen Taoyu,Chen Hongyan.FoxM1 down-regulation promotes sensitivity of laryngeal carcinoma Hep-2 cells to cisplatin[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(16):1603-1608. DOI：

摘要

目的探讨下调FoxM1表达对人喉癌Hep-2细胞顺铂敏感性的影响及其可能机制。方法分别选用FoxM1 siRNA以及FoxM1特异性抑制剂（硫链丝菌肽）下调Hep-2细胞FoxM1表达。实时定量PCR、Western blot检测siRNA或硫链丝菌肽处理细胞后FoxM1 mRNA、蛋白表达量；MTT法检测下调FoxM1表达后Hep-2细胞的顺铂敏感性；流式细胞术检测下调FoxM1表达后顺铂诱导的凋亡率变化；实时定量PCR、Western blot检测顺铂作用于FoxM1下调组及对照组细胞，其FoxM1 mRNA、蛋白及凋亡相关蛋白Bcl-2、Bax表达变化。结果 siRNA及硫链丝菌肽均能下调FoxM1表达（P0.05)；两种方式均能降低顺铂作用下细胞存活率以及IC

50

[NC组顺铂IC

50

=（2.609±0.102）μg/mL，干扰组IC

50

=（0.771±0.058）μg/mL，P0.05；对照组顺铂IC

50

=（2.142±0.198）μg/mL，抑制剂组IC

50

=（0.773±0.063）μg/mL，P0.05

]

，siRNA法处理后NC组、干扰组、NC+顺铂组、干扰+顺铂组凋亡率依次为（4.197±0.273）%、（12.553±0.183）%、（37.465±4.305）%、（82.373±7.214）%，干扰+顺铂组凋亡率显著升高（P0.05）；抑制剂处理后对照组、抑制剂组、顺铂组、抑制剂+顺铂组凋亡率依次为（2.343±0.194）%、（10.127±0.479）%、（35.075±1.995）%、（62.843±1.824）%，抑制剂+顺铂组凋亡率显著升高（P0.05）；下调FoxM1表达，凋亡抑制蛋白Bcl-2下调，促凋亡蛋白Bax表达上调（P0.05)。结论下调FoxM1表达可提高Hep-2细胞对顺铂的敏感性，其机制可能与凋亡相关蛋白Bcl-2下调、Bax上调相关。

Abstract

Objective To determine the effect of down-regulation of forkhead box protein M1 (FoxM1) on the cisplatin sensitivity of human laryngeal carcinoma Hep-2 cells and investigate the potential mech

anisms. Methods Small interfering RNA (siRNA) and FoxM1 inhibitor thiostrepton were used respectively to suppress FoxM1 expression in Hep-2 cells. The expression of FoxM1 at mRNA and protein levels was detected by qRT-PCR and Western blotting respectively. Cell viability and apoptosis of Hep-2 cells were detected by MTT assay and flow cytometry. Furthermore

qRT-PCR and Western blotting were used to investigate the changes of FoxM1 in Hep-2 cells with FoxM1 suppression and cisplatin treatment. The changes of apoptosis-related proteins were detected by Western blotting. Results Both of siRNA and thiostrepton suppressed FoxM1 expression

reduced the cell survival after cisplatin treatment and IC

50

(cisplatin treated normal cells IC

50

=2.609±0.102 g/mL

siRNA infected cells IC

50

=0.771±0.058 g/mL

P0.05; cisplatin treated cells IC

50

=2.142±0.198 g/mL

thiostrepton treated cells IC

50

=0.773±0.063 g/mL

P0.05). The apoptotic rate was (4.197±0.273)%

(12.553±0.183)%

(37.465±4.305)% and (82.373±7.214) % respectively in the normal Hep-2 cells and the cells with siRNA infection

cisplatin treatment and infection plus cisplatin treatment

with that of the latter group of cells the highest (P0.05). The rate was (2.343 3±0.193 6)%

(10.127±0.479)%

(35.075±1.995)% and (62.843±1.824)% separately in the normal Hep-2 cells and the cells after thiostrepton treatment

cisplatin treatment and thiostrepton plus cisplatin treatment

with that of the latter group of cells the highest (P0.05). Down-regulation of FoxM1 inhibited the expression of Bcl-2 and up-regulated that of Bax. Conclusion FoxM1 promotes the sensitivity of Hep-2 cells to cisplatin

which potentially is due to its down-regulation of Bcl-2 and up-regulation of Bax.

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