Sunitinib inhibits proliferation of head and neck cell line PCI-13 by blocking STAT3 signal pathway

贾志宇; 赵云转; 屈鹏飞; 张英怀; Lim Chweeming; Robert L Ferris

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Sunitinib inhibits proliferation of head and neck cell line PCI-13 by blocking STAT3 signal pathway

更新时间：2026-01-09

- Sunitinib inhibits proliferation of head and neck cell line PCI-13 by blocking STAT3 signal pathway
- Journal of Army Medical University Vol. 36, Issue 1, Pages: 55-58(2014)
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  CLC： R73-361;R739.91;R979.1
- Published：2014
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贾志宇,赵云转,屈鹏飞,张英怀,Lim Chweeming,Robert L Ferris.舒尼替尼阻断STAT3通路抑制头颈鳞癌细胞PCI-13增殖[J].陆军军医大学学报(原第三军医大学学报),2014,36(01):55-58.

　Jia Zhiyu,Zhao Yunzhuan,Qu Pengfei,Zhang Yinghuai,Lim Chweeming,Robert L Ferris.Sunitinib inhibits proliferation of head and neck cell line PCI-13 by blocking STAT3 signal pathway[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(01):55-58.
贾志宇,赵云转,屈鹏飞,张英怀,Lim Chweeming,Robert L Ferris.舒尼替尼阻断STAT3通路抑制头颈鳞癌细胞PCI-13增殖[J].陆军军医大学学报(原第三军医大学学报),2014,36(01):55-58. DOI：

　Jia Zhiyu,Zhao Yunzhuan,Qu Pengfei,Zhang Yinghuai,Lim Chweeming,Robert L Ferris.Sunitinib inhibits proliferation of head and neck cell line PCI-13 by blocking STAT3 signal pathway[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(01):55-58. DOI：

摘要

目的体外研究舒尼替尼对头颈鳞癌细胞系PCI-13增殖和凋亡的影响，并观察STAT1、STAT3在凋亡过程中的变化，探讨STAT3通路在舒尼替尼诱导肿瘤细胞凋亡中的作用。方法体外培养PCI-13细胞，用不同浓度的舒尼替尼处理24、48、72 h后，应用MTT比色实验，倒置显微镜、Wright-Giemsa染色、流式细胞术检测和观察PCI-13的生长抑制率和凋亡情况。细胞经血清饥饿后，分别用0、1、2、4 μmol/L的舒尼替尼处理2、8、16和24 h，采用流式细胞术检测p-STAT1和3的表达，并设阴性和阳性对照组。结果舒尼替尼可明显抑制PCI-13细胞的增殖，其最高抑制率可达92%，各浓度用药组不同处理时间之间生长抑制率有显著差异（

0.05），抑制率呈时间-浓度依赖性。同时舒尼替尼可诱导PCI-13细胞凋亡，凋亡率随处理时间延长和药物浓度增加而上升（

0.05）。舒尼替尼不影响p-STAT1的表达（

0.05），但是可以显著抑制p-STAT3的表达，这种抑制存在浓度依赖性（

0.05）。结论舒尼替尼不但能够抑制PCI-13细胞增殖，诱导其凋亡，而且能够抑制PCI-13细胞中STAT3的磷酸化水平，减少其激活。提示舒尼替尼诱导PCI-13细胞凋亡可能由STAT/JAK途径介导。

Abstract

Objective To evaluate the effect of sunitinib on the proliferation and expression of phosphorylating-signal transducer and activator of transcription1 and 3 (STAT1

STAT3) in the head and neck cancer cell line PCI-13 in order to determine the role of STAT3 pathway in the antitumor activity of sunitinib. Methods PCI-13 cells were treated with different concentrations of sunitinib (1.25

2.5

10 and 20 μmol/L) for 24

48 and 72 h. Then MTT assay

nversion phase contrast microscopy

Wright-Giemsa staining and flow cytometry were used to calculate the growth inhibitory rate and to observe the apoptosis of PCI-13 cells. PCI-13 cells were respectively treated with 0

2 and 4 μmol/L sunitinib for 2

16 and 24 h after 48 hours’ sera starving. Then phosphorylated-STAT1 and 3 were detected with flow cytometry. Results Sunitinib significantly inhibited the growth of PCI-13 cells in a time- and dose-dependent manner （

0.05）and the highest inhibitory rate was 92%. Meanwhile

sunitinib also significantly induced apoptosis in PCI-13 cells

and the apoptotic rate was increased in a time- and dose-dependent manner（

0.05）. Sunitinib had no effect on the expression of p-STAT1（

0.05）

but significantly suppressed the expression of p-STAT3 in a dose-dependent manner（

0.05）. Conclusion Sunitib not only inhibits the proliferation and induces the apoptosis of PCI-13 cells in a time- and dose-dependent manner

but also inhibits the phosphorylation and actitvity of STAT3

suggesting that sunitinib might induce apoptosis in PCI-13 cells by STAT/JAK pathway.

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