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Updated: Jan 23, 2026

In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines
Published on: March 5, 2019
Formyl-peptide receptor 2 suppresses proliferation, migration and invasion in human extravillous trophoblastic cells
Shenzhi Zhao1, Tingting Liao2, Tong Zhou2
1The Second Clinical College, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325027, People's Republic of China.
Abstract:
Although FPR2 receptor is distributed in the endometrium and placenta, its function in human extravillous trophoblastic (TEV-1) cells still remains enigmatic. In this study, overexpression of FPR2 was performed in TEV-1 cells. Then, CCK8 transwell and wound healing assays were used to assess the cell proliferation, migration and invasion, respectively. The results showed that FPR2 overexpression significantly inhibited proliferation, invasion and migration in TEV-1 cells. In addition, FPR2 overexpression significantly decreased mRNA and protein levels of integrin-linked kinase (ILK), nuclear factor-kappa B (NF--κB), matrix metalloproteinase 9 (MMP9) and vascular endothelial growth factor (VEGF) in TEV-1 cells. These findings indicated that FPR2 overexpression alters proliferation, migration and invasion in human extravillous trophoblastic cellsthrough the ILK/NF-κB signaling pathway; ideal FPR2 levels are important for TEV-1 cells functions.
Insights
Overexpressing the FPR2 receptor in human extravillous trophoblast (TEV-1) cells inhibited proliferation, migration, and invasion. This suggests ideal FPR2 levels are crucial for normal TEV-1 cell function.
Area of Science:
- Reproductive biology
- Cell biology
- Molecular signaling
Background:
- The function of the Formyl Peptide Receptor 2 (FPR2) in human extravillous trophoblast (TEV-1) cells is not well understood.
- FPR2 is known to be present in the endometrium and placenta.
Purpose of the Study:
- To investigate the role of FPR2 in regulating the proliferation, migration, and invasion of human extravillous trophoblast (TEV-1) cells.
- To elucidate the molecular mechanisms underlying FPR2's function in TEV-1 cells.
Main Methods:
- Overexpression of FPR2 in TEV-1 cells.
- Cell proliferation was assessed using CCK8 assays.
- Cell migration and invasion were evaluated using transwell and wound healing assays.
- mRNA and protein levels of key signaling molecules were measured.
Main Results:
- FPR2 overexpression significantly inhibited TEV-1 cell proliferation, migration, and invasion.
- FPR2 overexpression led to decreased expression of integrin-linked kinase (ILK), nuclear factor-kappa B (NF-κB), matrix metalloproteinase 9 (MMP9), and vascular endothelial growth factor (VEGF).
- These effects were mediated through the ILK/NF-κB signaling pathway.
Conclusions:
- FPR2 plays a critical role in regulating the functional properties of human extravillous trophoblast (TEV-1) cells.
- Maintaining optimal FPR2 levels is essential for proper TEV-1 cell function during placental development.
- The ILK/NF-κB signaling pathway is implicated in the mechanism by which FPR2 influences TEV-1 cell behavior.
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