缺氧卵巢癌细胞分化过程中LSD1表达的改变

Expression of LSD1 in ovarian cancer differenting into vasculogenic in role of hypoxia

目的通过体外实验研究缺氧状态卵巢上皮性癌细胞分化为内皮细胞中的LSD1的表达情况。方法常氧和缺氧培养OVCAR-3细胞,显微镜观察OVCAR-3细胞拟态血管形态。应用Western印迹检测经处理后OVCAR-3细胞株中LSD1的表达变化,并检测组蛋白的H3K4(2m)甲基化水平。结果在三维培养卵巢上皮性癌细胞系OVCAR-3时缺氧可诱导拟态血管的形成。Westem印迹检测出变化,缺氧条件下相对常氧条件下的LSD1表达量增加(2.91±0.2),且差异有统计学意义(P<0.05),组蛋白H3K4(2m)甲基化水平下降明显(0.22±0.03),且差异有统计学意义(P<0.05)。结论缺氧可诱导上皮性卵巢癌OVCAR3细胞LSD1表达上升,同时在体外三维立体培养中形成拟态血管。

Objective To explore the effect of hypoxia and HCG in vasculogenic mimicry( VM) of ovarian cancer in vitro. Methods Incubation of epithelial ovarian cancer cells OVCAR-3 was used to evaluate the effect of ox on VM formation. VM was identified by morphological observation. Potential formation of tumor channels was observed by light microscopy. Expression of LSD1 and it's histone demethlyation〔H3K4( 2m) 〕were detected by western blot at 4 days. Results The present study had shown that OVCAR-3 cells formed vessel-like network structures by exposed to 1% oxygen in three-dimensional culture. The expression level of LSD1 under normoxic condition was significantly higher than that of control( 2. 91±0. 2,P<0. 05). Yet the level of histone demethlyation H3K4( 2m) was decrease significantly( 0. 22±0. 03,P<0. 05). Conclusions Hypoxia can induce upregulation of LSD1 expression as well as VM formation in OVCAR-3.