甲酸基肽受体2抑制滋养细胞增殖侵袭功能的机制

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摘要目的：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Western blot检测核转录因子（NF-κB）和基质金属蛋白酶9（MMP9）mRNA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 mRNA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。

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	赵慎之
	黄贤苹
	项慧秋
	廖婷婷
	陈佳佳
	许张晔

关键词 ：脂氧素A4, 甲酸基肽受体2, 绒毛外滋养细胞, 细胞增殖, 细胞运动, 细胞侵袭

Abstract：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-ĸB 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-ĸB 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-ĸB/MMP9 pathway in TEV-1 cells.

Key words： lipoxin A4 formyl peptide receptor 2 extravillous trophoblast cell proliferation cell movement cell invasion

基金资助:国家自然科学基金资助项目（81471493，81771555）；浙江省自然科学基金资助项目（LY14H040014）。

通讯作者: 许张晔，主任医师，副教授，硕士生导师，Email：531953862@qq.com。

作者简介: 赵慎之（1999-），男，浙江温州人，本科生。

链接本文:

https://xb.wmu.edu.cn/CN/ 或 https://xb.wmu.edu.cn/CN/Y2018/V48/I8/552

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