DOC-2对卵巢癌细胞HO-8910致瘤力的影响

The impact of DOC-2 expression on the tumorigenesis of human ovarian cancer cell line(HO-8910)

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 and purpose： Studies have shown that DOC-2 could work as a potential tumor suppressor geue, and the role of DOC-2 in terms of the inhibition of cell growth and its mechanism remain unknown. Our paper is to investigate the effect and mechanism of DOC-2 expression on the tumorigenesis viability of ovarian cancer cell line HO-8910 from the aspects of clone efficiency, cell cycle and animal model test. Methods： Three cell lines were used including HO- 8910, 8910-P93（ transfected with DOC-2 gene） and 8910-pcDNA3.1（ transfected with the vector pcDNA3.1）. Firstly, soft agar method was used to measure the clone efficiency. The cell cycle were analyzed by flow cytometer. The tumorigenesis viability was compared by athymic mouse test. Results： After being transfected with DOC-2 gene, the clone efficiency of 8910-P93 was markedly reduced. There was no difference between the 8910-pcDNA3.1 and HO-8910. GI and G2 arrest were observed for 8910-P93. The athymic mouse test showed that the neoplasm derived from 8910-P93 was much smaller than that in the controls. Conclusions： DOC-2 could inhibit the tumorigenesis viability of human ovarian cancer line HO- 8910.