MiR-506通过PI3K/AKT信号通路调控人绒毛膜癌细胞增殖、迁移和侵袭

MiR-506 regulates the proliferation,migration and invasion of human choriocarcinoma cells through the PI3K/AKT signaling pathway

目的探讨MiR-506是否通过PI3K/AKT通路对人绒毛膜癌细胞JEG-3的增殖、迁移、侵袭和凋亡发挥调控作用。方法采用qRT-PCR法测定绒毛膜滋养层细胞HTR8/Svneo和绒毛膜癌细胞JEG-3中MiR-506的表达水平,将JEG-3细胞分组后转染MiR-506模拟物或抑制物后进行培养,采用CCK-8法测定细胞增殖情况,采用流式细胞术测定各组细胞凋亡情况,采用Western blot法测定PI3K/AKT通路相关蛋白表达情况。结果JEG-3细胞中MiR-506表达水平较HTR8/Svneo细胞降低;MiR-506模拟物组JEG-3细胞中MiR-506表达水平升高,MiR-506抑制物组MiR-506表达水平降低;MiR-506模拟物组24 h、48 h、72 h时吸光度增加,而MiR-506抑制物组吸光度显著降低;MiR-506模拟物组细胞凋亡数量升高(P<0.05),而MiR-506抑制物组细胞凋亡数量降低(P<0.05);MiR-506模拟物组PI3K和AKT蛋白表达水平降低(P<0.05),MiR-506抑制物组PI3K和AKT蛋白表达水平增加(P<0.05)。结论MiR-506是绒毛膜癌的抑癌基因,可能通过调节PI3K/AKT通路对绒毛膜癌细胞的增殖、迁移、侵袭和凋亡发挥调节作用。

Objective To investigate the regulation of MiR-506 on proliferation,migration,invasion and apoptosis of choriocarcinoma JEG-3 cells via PI3K/AKT signal pathway.Methods qRT-PCR was used to determine MiR-506 in JEG-3 cells and normal HTR8/Svneo cells.JEG-3 cells were cultured after transfection and divided into different groups.CCK 8 method was used to determine cell proliferation.Flow cytometry was used to determine cell apoptosis.Western-blot were used to determine and protein related to PI3K/AKT signal pathway.Results The expression of MiR-506 in JEG-3 cells was increased compared with that in HTR8/Svneo cells;MiR-506 in MiR-506 mimics group increased,while MiR-506 in MiR-506 inhibitor group decreased.The absorbance value in MiR-506 mimic group at 24 h,48 h and 72 h decreased,while absorbance value in MiR-506 inhibitor group at 24 h,48 h and 72 h increased.The apoptosis rate in MiR-506 group increased,while the apoptosis rate in MiR-506 inhibitor group decreased.The mRNA and protein levels of PI3K and AKT in MiR-506 mimic group decreased,while the mRNA and protein levels of PI3K and AKT in MiR-506 inhibitor group increased.Conclusion MiR-506 is a tumor suppressor gene of choriocarcinoma,which may regulate the proliferation,migration,invasion and apoptosis of choriocarcinoma of choriocarcinoma cells Via the PI3K/AKT signal pathway.