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论文摘要

外源性碱性成纤维细胞生长因子对人腺样囊性癌细胞株ACC-2增殖和细胞外信号调节激酶、CyclinD1及p21~(waf/cip1)通路的影响

Effects of basic fibroblast growth factor on the prolifer ation of human salivary adenoid cystic car cinoma cell line ACC- 2 and extr acellular signal- r egulated kinase

作者:丁蕾 朱声荣 谢三祥 吴祥冰

Author:DING Lei, ZHU Sheng- rong, XIE San- xiang, WU Xiang- bing

收稿日期:2008-04-25          年卷(期)页码:2008,26(02):118-

期刊名称:华西口腔医学杂志

Journal Name:West China Journal of Stomatology

关键字:碱性成纤维细胞生长因子,腺样囊性癌,细胞外信号调节激酶,

Key words:basic fibroblast growth factor,adenoid cystic carcinoma,extracellular signal- regulated kinase,

基金项目:

中文摘要

目的腺样囊性癌(ACC)是最常见的唾液腺恶性肿瘤之一。本研究拟观察碱性成纤维细胞生长因子 (bFGF)对人ACC- 2细胞增殖及细胞外信号调节激酶(ERK)、Cyclin D1及p21waf/cip1信号通路的影响。方法培养人 ACC- 2细胞,MTT比色法测定不同浓度的外源性bFGF对细胞增殖的影响;采用ERK活性测定试剂盒测定ERK活性; 免疫印迹法测定p- ERK1/2和下游的Cyclin D1及p21waf/cip1表达。并观察丝裂原蛋白活化激酶激酶(MEK)抑制剂U0126对 上述指标的干预作用。结果MTT实验显示bFGF明显增强ACC- 2细胞增殖,bFGF可上调ERK活性,免疫印迹法显 示bFGF明显增强p- ERK1/2、Cyclin D1表达及抑制p21waf/cip1表达。U0126可抑制bFGF的以上效应。结论bFGF可促进 人ACC- 2细胞增殖,其途径与上调p- ERK1/2活性、抑制p21waf/cip1表达进而增强Cyclin D1表达有关。本研究为ACC的发 病机制及治疗提供新思路。

英文摘要

Objective To investigate the effects of basic fibroblast growth factor(bFGF) on the proliferation of human salivary adenoid cystic carcinoma(ACC)cell line ACC- 2 in vitro. Methods The effect of ectogenic bFGF on proliferation of ACC- 2 was observed by MTT assay. Extracellular signal- regulated kinase(ERK)activity was measured by immuno- precipitation. p- ERK1/2, Cyclin D1 and p21waf/cip1 expression were assessed by Western blot. Results bFGF could enhance the proliferation of ACC- 2. Stimulated by bFGF, the proliferation ratio increased significantly. The intracellular ERK activity, p- ERK1/2 and Cyclin D1 expression were increased, while p21waf/cip1 expression was inhibited by different concentrations of bFGF. The above effects of bFGF could be attenuated by MEK inhibitor U0126. Conclusion bFGF stimulates the proliferation of ACC- 2 in a dose dependent manner. The proliferation effect of bFGF may be due to up- regulating ERK, Cyclin D1 and p21waf/cip1 signaling pathway. This research can help us to explore a new pathogenesis and therapy of the ACC.

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