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目的:探讨抑制前列腺素E2合酶1(mPGES-1)表达对人急性白血病K562细胞在裸鼠体内成瘤的影响及其可能的机制。方法:通过shRNA干扰技术下调K562细胞中mPGES-1表达,实验设立了如下研究小组:①干扰组(KD),②阴性细胞(NC)非特异序列shRNA干扰组;③未处理组(CON组);应用Western blot法检测β-catenin和cyclin D1在3组细胞中的表达;构建K562细胞人-裸鼠移植瘤模型,观察移植瘤的生长情况;应用HE染色观察各组肿瘤组织的结构;应用免疫组织化学法检测β-catenin和cyclin D1的表达水平。结果:与CON组和NC组比较,细胞体外实验结果显示KD组β-catenin和cyclin D1表达量减少(P<0.05);动物体内实验结果显示,KD组瘤体生长明显减慢,移植瘤体积明显缩小,重量明显减轻(P<0.01);HE染色显示,KD组细胞排列相对松散,间质较多,肿瘤细胞核小,细胞质较少;免疫组织化学检测显示,KD组β-catenin和cyclin D1表达量明显下降(P<0.05)。结论:下调mPGES-1表达能显著抑制人急性白血病K562细胞在裸鼠体内成瘤,其机制可能与抑制β-catenin和cyclinD1表达相关。
AIM: To investigate the effect of prostaglandin E2 synthase 1 (mPGES-1) on tumorigenesis of human acute myeloid leukemia K562 cells in nude mice and its possible mechanism. Methods: The expression of mPGES-1 in K562 cells was downregulated by shRNA interference. The following groups were established: ① interference group (KD), ② negative group (NC) nonspecific shRNA interference group; ③ untreated group Western blot was used to detect the expression of β-catenin and cyclin D1 in 3 groups of cells. The K562 cells were transplanted into xenografts in nude mice to observe the growth of the transplanted tumor. HE staining was used to observe the structure of the tumor tissues. The expression of β-catenin and cyclin D1 were detected by immunohistochemistry. Results: Compared with CON group and NC group, the results of in vitro experiments showed that the expression of β-catenin and cyclin D1 in KD group decreased (P <0.05). The results of in vivo experiments in KD group showed that the growth of tumor in KD group was significantly slowed down, (P <0.01). HE staining showed that the cells in KD group were relatively loosely arranged with more interstitial nuclei and less cytoplasm. Immunohistochemistry showed that the expression of β-catenin and cyclin D1 The expression level decreased significantly (P <0.05). CONCLUSION: Down-regulation of mPGES-1 expression can significantly inhibit the tumorigenesis of human acute myeloid leukemia K562 cells in nude mice, which may be related to the inhibition of the expression of β-catenin and cyclinD1.