In vitro experiments revealed that miR‑203 overexpression significantly downregulated VEGFA expression and inhibited the proliferation, migration and invasion ability of HTR‑8/SVneo cells.
HTR-8/SVneo cells were exposed to unflavored e-cigarette vapour-conditioned media with and without nicotine to assess cell viability, proliferation, migration (wound healing assay), invasion (transwell extracellular matrix invasion assay), and tube formation, a surrogate for angiogenesis.
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.
Using the HTR-8/SVneo cell line as a model system, we found that overexpression of EIF5A1 promotes trophoblast proliferation, migration and invasion in vitro.
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.
Overexpressed miR-141-3p in HTR-8/SVneo cells contributed to increased cell proliferation, invasion, and migration. miR-141-3p inhibition in HTR-8/SVneo cells resulted in decreased cell proliferation and invasion.
Meanwhile, increased proliferation, enhanced invasion and decreased apoptosis of HTR-8/SVneo cells was observed in miR-145 mimic groups compared with mimic control group.
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.
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.
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.
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>).
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.
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.
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.