甲酸基肽受体2抑制滋养细胞增殖侵袭功能的机制

The mechanism of FPR2 in suppressing the proliferation, migration and invasion of human extravillous trophoblastic cells

目的:研究甲酸基肽受体2(FPR2)对滋养细胞(TEV-1)增殖侵袭功能的调控作用及其机制。方法:构建FPR2慢病毒载体后,转染人TEV-1细胞来过表达FPR2;采用MTT法、Transwell法和划痕实验检测细胞的增殖、迁移和侵袭能力;采用RT-PCR和Westernblot检测核转录因子(NF-κB)和基质金属蛋白酶9(MMP9)m RNA和蛋白表达。结果:过表达FPR2后,TEV-1细胞的FPR2基因和蛋白的表达水平显著升高(P<0.001),证明过表达FPR2成功。过表达FPR2后,TEV-1细胞的增殖能力受到显著抑制(P<0.01),TEV-1细胞侵袭能力明显下降(P<0.05),TEV-1细胞迁移能力显著下降(P<0.01)。过表达FPR2转染TEV-1细胞后,NF-κB和MMP9的m RNA和蛋白水平显著下降(P<0.001)。结论:FPR2可能通过NF-κB/MMP9信号通路抑制TEV-1细胞的增殖、迁移和侵袭功能。

Objective： To explore the preliminary mechanism and effect of FPR2 on the proliferation, migration and invasion of human extravillous trophoblastic cells（TEV-1）. Methods： Overexpression of FPR2 RNA was constructed and transfected into human TEV-1 cells. MTT assay, transwell assay and scarification test were used to detect the cell proliferation, migration and invasion. RT-PCR and Western blot was used to detect the expression of NF-.B and MMP9 mRNA and protein. Results： Over-expression of FPR2 significantly increased the expression levels of FPR2 mRNA and protein in TEV-1 cells（P〈0.001）, indicating that the transfection was successful.Over-expression of FPR2 gene significantly inhibited the proliferation, invasion（P〈0.01） and migration of TEV-1 cells（P〈0.05）. Over-expression of FPR2 gene significantly decreased the mRNA and protein levels of NF-.B and MMP9 in TEV-1 cells（P〈0.001）. Conclusion： These findings indicated that over-expression of FPR2 gene may perturb proliferation, migration and invasion through NF-.B/MMP9 pathway in TEV-1 cells.