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背景与目的:作为近年发现的新的肿瘤抑制基因,DOC-2的作用机制还不完全清楚。本实验的目的在于观察DOC-2转染后对卵巢癌细胞系HO-8910在克隆形成率、细胞周期、裸鼠致瘤能力等方面的影响,并对其作用机制进行初步探讨。方法:实验分3组:卵巢癌细胞系HO-8910(无DOC-2基因的表达)、8910-P93(经转染并表达DOC-2基因)、8910-pcDNA3.1(转染空载体pcDNA3.1),首先通过软琼脂克隆形成实验比较3组细胞克隆形成率的差异,之后利用流式细胞仪观察其细胞周期的变化,最后用裸鼠荷瘤实验进一步验证DOC-2对肿瘤细胞致瘤能力的影响。结果:卵巢癌细胞系HO-8910在转染DOC-2后其克隆形成率明显降低,与转染前差异明显(P<0.05),同时G1和G2期细胞明显增多而S期细胞明显减少,移植瘤裸鼠荷瘤实验显示HO-8910-P93细胞在裸鼠体内生长缓慢,肿瘤体积及重量均明显低于对照组(P<0.05)。结论:DOC-2基因能明显抑制卵巢癌细胞系HO-8910的致瘤力。
BACKGROUND & AIM: As a new tumor suppressor gene discovered in recent years, the mechanism of action of DOC-2 is not fully understood. The purpose of this experiment is to observe the effect of DOC-2 transfection on the formation rate of ovarian cancer cell line HO-8910, the cell cycle and the tumorigenicity of nude mice, and to explore its mechanism. METHODS: The experiment was divided into three groups: ovarian cancer cell line HO-8910 (no DOC-2 gene expression), 8910-P93 (transfected and expressed DOC-2 gene), 8910- pcDNA3.1 .1) .Firstly, the difference of colony formation rate of three groups was compared by soft agar colony formation assay. Then the change of cell cycle was observed by flow cytometry. Finally, the effect of DOC-2 on tumor cells induced by DOC-2 Tumor capacity effects. Results: Clone formation rate of ovarian cancer cell line HO-8910 after transfection with DOC-2 was significantly lower than that before transfection (P <0.05). At the same time, the cells in G1 and G2 phases increased significantly and the cells in S phase decreased significantly, The transplanted tumor in nude mice tumor-bearing experiments showed that HO-8910-P93 cells in slow growth in nude mice, tumor volume and weight were significantly lower than the control group (P <0.05). Conclusion: DOC-2 gene can significantly inhibit the tumorigenicity of ovarian cancer cell line HO-8910.