复方中药白龙对G<sub>1</sub>期人胃癌细胞中抑癌基因的影响及与PKA信号通路的相关性

Effect of Compound Chinese Drug Bailong on the Expression of Tumor Suppressor Genes and Relationship with Prekallikrein Activator Signal Pathway in Human Gastric Carcinoma BGC82-3 Cell Line

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中文关键词: 复方中药白龙 G₁期 BGC82-3 CKI p16^INK4a cAMP-PKA信号通路 PKA抑制剂

英文关键词:Bailong G 1 phase BGC82 3 CKI p16 INK4a cAMP PKA pathway PKA inhibitor

基金项目:国家自然科学基金!No.39480 0 2 6 ,39780 0 1 4;北京市自然科学基金!No.7961 0 0 1

作者	单位
刘军	Liu Jun, Liu Huitu, Liang Yunyan, et al. Department of Cell Biology, Medical University, Beijing Institute for Cancer Research (100034
柳惠图	Liu Jun, Liu Huitu, Liang Yunyan, et al. Department of Cell Biology, Medical University, Beijing Institute for Cancer Research (100034
梁云燕	Liu Jun, Liu Huitu, Liang Yunyan, et al. Department of Cell Biology, Medical University, Beijing Institute for Cancer Research (100034
王代树	Liu Jun, Liu Huitu, Liang Yunyan, et al. Department of Cell Biology, Medical University, Beijing Institute for Cancer Research (100034

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中文摘要:

目的 :探讨复方中药白龙 (简称白龙 )对人胃癌BGC82 3G1期细胞周期蛋白激酶抑制因子(CKI) p16INK4a、p2 1以及Rb、c myc等基因转录的影响和cAMP PKA信号通路的调节关系。方法 :通过实验室常规分子生物学手段 (细胞同步化、分子杂交———Northern杂交、Western杂交等 )检测相关基因的表达变化。结果 :白龙对G1期细胞p16INK4a表达有强烈促进作用 ,mRNA和蛋白水平均显著升高 ;处理细胞的同时加入PKA抑制剂阻断该信号通路后 ,白龙作用丧失 ,p16INK4a mRNA和蛋白水平明显下降 ;白龙还可以促进抑癌基因Rb、p2 1的mRNA表达和抑制癌基因c mycmRNA的表达 ;同样在白龙作用的同时阻断该信号通路 ,则白龙的上述作用随之丧失。结论 :白龙可以通过影响BGC82 3G1期细胞中众多抑癌基因 (包括p16INK4a、p2 1、Rb)和癌基因 (包括c myc)的转录发挥其抑瘤生理效应 ,而这种变化发生的机理是与cAMP PKA信号通路的调节机制密切相关的。

英文摘要:

Objective: To study the effect of compound Chinese drug Bailong on the transcription of Cyclin Dependent Kinase Inhibitor (CKI) p16 INK4a , p21 and Rb, c myc genes, and the relationship between gene expression and cAMP PKA pathway. Methods: Using the traditional molecular biology methods (cell synchronization, molecular hybridization——Western blotting, Northern blotting, etc.) examine the gene expression. Results: Bailong promoted the expression (both mRNA and protein) of p16 INK4a obviously in G 1 phase cells. When prekallikrein (PKA) inhibitor was added in the cells which were treated by Bailong, the mRNA and protein level of p16 INK4a decreased. It was shown that the inhibited proliferation of BGC82 3 cell by Bailong may come from the enhanced p16 INK4a gene expression in G 1 phase. Being same as p16 INK4a , tumor suppressor genes Rb, p21 and oncogene c myc expression were all affected by Bailong. When PKA inhibitor was added, the results were reversed. Conclusion: Bailong can affect many anticancer genes (including p16 INK4a , p21 and Rb genes) and oncogenes (including c myc) transcription by regulating cAMP PKA pathway.

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