Mechanistically, c-Myc bound to the BMAL1 promoter and induced BMAL1 transcription, both of which further activated matrix metalloproteinase 2/9 (MMP2/9) and facilitated migration and invasion in HTR-8/SVneo cells.
Treatment of HTR-8/SVneo trophoblasts with serum from ozone-exposed dams for 16-h downregulated metabolic capacity, wound-closure, and invasion through a Matrigel membrane compared with both air-serum and fetal bovine serum-treated cells.
Induction of miR-141 by hypoxia promotes apoptosis, and inhibits the invasion and vascularization capabilities of HTR-8/SVneo cells by suppressing the CXCL12β and CXCR2/4 signaling pathways.
HTR-8/SVneo cell migration and invasion, and invasion by isolated trophoblast cells in primary culture were significantly reduced in the presence of I<sub>47,</sub> which could be restored by rhgalectin-3.
Inhibition of STAT-1 activity by fludarabine and STAT-3 activity by Stattic also leads to a decrease in H<sub>2</sub> O<sub>2</sub> -mediated increase in HTR-8/SVneo cell invasion.
A Transwell invasion assay and wound healing assay revealed that overexpression of FAM99A promoted invasion and migration of HTR‑8/SVneo cells; conversely, knockdown of FAM99A suppressed the invasive and migratory abilities of HTR‑8/SVneo cells.
Further analysis demonstrated that lncRNA MEG3 overexpression significantly inhibited HTR-8/SVneo cell viability, and prevented cell migration and invasion in addition to inducing cell apoptosis.
Meanwhile, HTR-8/SVneo cells incubated with Hemin showed increased invasion function against the destruction of hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>).
Our results showed that aspirin promoted trophoblast invasion not only in HTR-8/SVneo and JAR cells, but also in isolated cytotrophoblasts. sFlt-1 production was repressed by aspirin in a dose-dependent manner.
Attenuation of MIF by siRNA reduced HTR-8/SVneo cell invasion through Matrigel (59 % of control), expression of integrin α<sub>1</sub> (86 % of control) and levels of MMP2 and MMP9 (87 % and 57 % of control, respectively).
This study aimed to explore the role of the H19/let-7/ITGB3 axis in regulating trophoblastic spheroid adhesion and in vitro invasion ability using the HTR-8/SVneo cell line and to investigate the expression levels of lncRNA H19 and ITGB3 in human products of conception.
More importantly, both overexpression of miR-558 and knockdown of TIMP4 partially reversed the suppressive effects of Linc00261 overexpression on cell invasion and migration of HTR-8/SVneo cells.
Besides, while PI3K was blocked, the invasion and migration capability of HTR-8/SVneo cells and the expression of key kinases in PI3K/AKT/mTOR pathways were decreased significantly.
It was demonstrated that hsa-miR-181a-5p expression was upregulated in preeclamptic placentas and that it may trigger antiproliferation and inhibition of cell cycle progression, induce apoptosis, and suppress invasion in HTR-8/SVneo and JAR cells.
ERK1/2 and Akt signaling pathways mediate amphiregulin-induced upregulation of MMP9 mRNA and the MMP9/TIMP-1 ratio, which subsequently contribute to amphiregulin-promotion of HTR-8/SVneo cell invasion.