竹节香附素通过抑制JAK/STAT3信号转导通路抑制人子宫内膜癌HEC-1-B细胞的侵袭转移

目的:探讨竹节香附素对人子宫内膜癌HEC-1-B细胞的侵袭转移影响，以及JAK/STAT3信号转导通路在此过程中发挥的作用。方法:选取正常贴壁生长的对数期人子宫内膜癌HEC-1-B细胞，分成两组，一组用竹节香附素处理，为观察组；另一组用生理盐水处理，作为对照组。划痕实验比较两组的细胞在不同时间点的迁移情况；Transwell实验比较两组细胞的侵袭能力；CCK-8检测两组细胞的增殖能力；荧光定量PCR和Western blot检测细胞中Janus激酶（JAK）、信号转导子和转录激活子（STAT3）基因的表达情况。结果:48 h后，观察组的迁移距离小于对照组（P<0.05），Transwell实验观察组侵入下方小室的细胞数量低于对照组（P<0.05）。两组细胞在48 h内的细胞增殖结果差异并无统计学意义（P>0.05）。相比较对照组，荧光定量PCR和Western blot的结果均显示观察组的JAK和STAT3基因表达量下降（P<0.05）。结论:竹节香附素可显著抑制人子宫内膜癌HEC-1-B细胞的侵袭和转移能力，其机制可能通过调控JAK/STAT3信号通路而发挥作用。

Raddeanin inhibits the invasion and metastasis of HEC-1-B cells in human endometrial carcinoma by inhibiting the JAK/STAT3 signaling pathway

AIM: To investigate the effect of raddeanin on the invasion and metastasis of human endometrial carcinoma HEC-1-B cells, and the effects of the JAK/STAT3 signaling pathway. METHODS: HEC-1-B cells were selected from human endometrial carcinoma in logarithmic phase. One group was treated with raddeanin, which was the observation group. The other group was treated with saline as a control group. The scratch test was used to detect the cell migration at different time points in the two groups. The invasiveness of cells in two groups was compared by Transwell. The proliferation capacity of cells in two groups was measured by CCK-8. The expression of JAK and STAT3 in cells was detected by fluorescence quantitative PCR and Western blot. RESULTS:After 48 h, the migration distance of the observation group was shorter than that of the control group (P<0.05). The number of cells invading the lower compartment was less than that of the control group (P<0.05). The differences in cell proliferation between the two groups were not statistically significant during 48 h（P>0.05）. Compared with the control group, the results of fluorescence quantitative PCR and Western blot showed decreased expression of JAK and STAT3 genes in the observation group（P<0.05）. CONCLUSION: Raddeanin can significantly inhibit the invasion and metastasis of human endometrial carcinoma HEC-1-B cells and its mechanism may be through regulating the JAK/STAT3 signaling pathway.