Circular RNA circ_0111277 Attenuates Human Trophoblast Cell Invasion and Migration by Regulating miR-494/HTRA1/Notch-1 Signal Pathway in Pre-Eclampsia

Abstract Well-controlled trophoblast invasion into uterine decidua is a critical process for the normal development of placenta, which is tightly regulated by various factors produced within the trophoblast-endometrial microenvironment. CXCL14 is involved in tumor growth and metastasis, and its expression in placenta is temporally regulated during pregnancy. However, the role of CXCL14 in trophoblast function during human pregnancy is not clear. In this study, by using RT-PCR through human pregnancy, we found that CXCL14 was selectively expressed at early but not late pregnancy. Immunostaining revealed that CXCL14 proteins were strongly expressed in villous cytotrophoblasts and moderately in decidualized stromal cells but very weakly in syncytiotrophoblasts and extravillous trophoblasts. The effect of CXCL14 on trophoblast invasion were examined by using human villous explants cultured on Matrigel and further proved by invasion and migration assay of primary trophoblast cells and trophoblast cell line HTR-8/SVneo. Our data showed that CXCL14 significantly inhibited outgrowth of villous explant in vitro; this effect is due to suppression of trophoblast invasion and migration through regulating matrix metalloproteinases activities, whereas the trophoblast proliferation was not affected. Moreover, because a receptor for CXCL14 has not been identified, we performed further cell-specific CXCL14 binding activities with regard to different cell types within the maternal-fetal interface. Our data revealed that CXCL14 could specifically bind to trophoblast cells but not decidual cells from the maternal-fetal interface. These results suggest that CXCL14 plays an important role in regulating trophoblast invasion through an autocrine/paracrine manner during early pregnancy.

Download Full-text

Mesenchymal Stem Cells-Derived Exosomal H19 Promotes Trophoblast Cell Invasion and Migration by Down-Regulating Let-7b in Preeclampsia

SSRN Electronic Journal ◽

10.2139/ssrn.3422972 ◽

2019 ◽

Author(s):

Yang Chen ◽

Haiyan Ding ◽

Min Wei ◽

Wenhui Zha ◽

Shuang Guan ◽

...

Keyword(s):

Stem Cells ◽

Mesenchymal Stem Cells ◽

Cell Invasion ◽

Trophoblast Cell ◽

Invasion And Migration ◽

And Migration

Download Full-text

Effects of Epidermal Growth Factor Receptor Signal Pathway on Proliferation, Invasion and E-Cadherin/Vimentin Protein Expression in Laryngeal Carcinoma Hep-2 Cells

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2021.2730 ◽

2021 ◽

Vol 11 (8) ◽

pp. 1595-1599

Author(s):

Tingting Wu ◽

Xuhong Zhou ◽

Linfeng Ye ◽

Shuang Li ◽

Jing Huang ◽

...

Keyword(s):

Cell Cycle ◽

Cell Invasion ◽

Laryngeal Carcinoma ◽

Growth Factor Receptor ◽

Signal Pathway ◽

Carcinoma Cells ◽

Invasion And Migration ◽

Epidermal Growth ◽

And Migration ◽

E Cadherin

Epidermal growth factor receptor (EGFR) is one transmembrane receptor with a high expression in more than 90% of head-neck squamous carcinoma cells. This study investigated the role of EGFR signal pathway on proliferation, invasion and expression of related proteins E-cadherin/Vimentin expression in laryngeal carcinoma cells. Laryngeal carcinoma Hep-2 cells were treated with EGFR agonist EGF or inhibitor Gefitinib followed by measuring cell cycle, proliferation index (PI) and apoptosis by flow cytometry. Transwell assay was employed for cell invasion and migration. Western blotting was further employed to test E-cadherin and Vimentin level. Compared to blank control group, EGF-treated cells had significantly lower S percentage of cell cycle at 6 h, 12 h and 24 h, plus higher PI. With prolonged incubation time, S ratio and PI were further significantly elevated, with more potent cell invasion and migration abilities, lower E-cadherin and Vimentin protein levels (p < 0.05). Gefitnib significantly elevated S ratio at 6 h, 12 h and 24 h cell cycle, reduced PI, invasion or migration ability, as upregulated E-cadherin and downregulated Vimentin protein (p < 0.05). Suppressing EGFR signal pathway could inhibit proliferation of laryngeal carcinoma cells, decrease cell invasion or migration, upregulate E-cadherin and downregulate Vimentin.

Download Full-text