LncRNA HOTAIR促进女性滋养层细胞迁移的机制

目的 探究长链非编码RNA HOTAIR对女性滋养层细胞系Swan 71和HTR-8/SVneo细胞迁移能力的影响以及潜在的分子机制。方法 采取特异性小干扰RNA敲低两种滋养层细胞系中HOTAIR后，采用划痕实验检测滋养层细胞迁移能力的改变，采用Western blot检测PI3K/AKT通路上蛋白的含量及其磷酸化水平的改变，采用Dunnett-t检验方法比较实验组与对照组数据的统计学差异。结果 与对照组比较，两种特异性小干扰RNA均可将Swan 71与HTR-8/SVneo细胞中HOTAIR的表达含量显著下调至30%以下；并且敲低HOTAIR后，两种滋养层细胞的迁移能力显著下降，细胞中PI3K/AKT蛋白总量不变，但其磷酸化水平都下调。结论 HOTAIR可促进女性滋养层细胞Swan 71与HTR-8/SVneo的迁移，上调PI3K与AKT蛋白的磷酸化水平，为后续开展更为深入的体内实验提供前期基础。

Long non-coding RNA HOTAIR promotes human trophoblast cell migration by activating PI3K/AKT pathway

To explore the effects of lncRNA HOTAIR on the migration of female trophoblast Swan 71 and HTR-8/SVneo cells and to discover its potential molecular mechanism. Methods SiRNAs were used to knock down HOTAIR in both trophoblast cell lines. Scratch tests were used to detect the migration ability of trophoblast cells. Western blot was used to detect the protein levels and phosphorylation levels of PI3 K and AKT. Dunnett test was used to compare the statistical differences between the experimental group and the control group.Results Compared with the control group, both siRNAs could significantly reduce the expression level of HOTAIR to less than 30% in both Swan 71 and HTR-8/SVneo cells. After knocking down HOTAIR, the migration ability of two trophoblast cells was significantly decreased, and the total protein levels of PI3 K and AKT protein in the cells remained unchanged, but its phosphorylation level was down-regulated.Conclusion HOTAIR can promote the migration of female trophoblast Swan 71 and HTR-8/SVneo cells, promote the phosphorylation level of PI3 K and AKT, and also provide scientific basis for further investigation HOTAIR functions.