摘要
目的研究SPRIDA(施普睿达)对荷H22肝癌小鼠基因表达的调节差异,探讨SPRIDA治疗小鼠肝癌的可能机制。方法运用基因表达谱芯片技术检测SPRIDA对荷瘤小鼠的基因表达调节,并对差异基因进行Pathway聚类和统计分析。结果SPRIDA作用前后表达有差异的基因共358条(占芯片基因总数的8.74%),其中172条(172/4096,4.20%)基因表达上调,186条(186/4096,4.54%)基因表达下调。经Pathway聚类分析,表达差异基因主要属于细胞凋亡、细胞周期、NK细胞介导的细胞毒、细胞黏附分子、肿瘤生长因子β、Wnt等信号通路。结论SPRIDA主要是通过影响肿瘤细胞周期进程、调节肿瘤细胞凋亡和黏附相关基因的表达等多种途径抑制肿瘤的增殖和转移。
Objective To study gene differential expression profiles by SPRIDA in tumor-bearing mice.To explore the potential molecular mechanism of anticancer for SPRIDA.Methods Gene expression profiles after treatment with SPRIDA in tumor-bearing mice were determined by Oligo chip technology as well as the pathway clustering and statistic analysis of single gene.Results 100 mg/kg SPRIDA treatment for 10 days caused the expression alteration of 358 genes （8.74% of total genes on the chip）.Among them,172（4.20%,172/4096）genes were up-regulated, and 186 （4. 54%, 186/4096） genes were down-regulated. Pathway analysis showed that they belonged to apoptosis, cell cycle, natural killer cell mediated cytotoxicity, cell adhesion molecules, TGF-beta and wnt signaling pathways. Conclusion The inhibitory effect of SPRIDA on tumor growth and metastasis were made by the influence of tumor cell cycle, regulation of apoptosis and cell adhesion genes, etc.
出处
《肿瘤防治研究》
CAS
CSCD
北大核心
2009年第12期1013-1015,共3页
Cancer Research on Prevention and Treatment
基金
科技部科研院所技术研究开发专项基金资助项目(2004EG136193)
天津市科技支撑计划重点项目(07ZCKFSH00200)
