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.
Over-expression of NTE in HTR-8/SVneo cells significantly promoted trophoblast cells migration and invasion and was associated with increased MMP-9 levels.
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.
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.
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.
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.
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>).
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.
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.
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.
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.
Furthermore, we treated HTR-8/SVneo cells with a shRNA Rac1 vector and the β-catenin inhibitor IWP-2 and explored Rac1 signalling pathway activation as well as the effects of Snail and β-catenin on trophoblast invasion.
Furthermore, the effect of LMP2 or proteasome on cell invasion was measured by using RNAi and inhibitors in a Matrigel invasion assay system in HTR-8/SVneo cells, a human invasive extravillous trophoblast cell line.
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.
Finally, inactivation of PPARγ pathway by either PPARγ inhibitors or PPARγ shRNA knockdown rescued the MEHP-induced inhibited invasion of HTR-8/SVneo cells, which is accompanied by the recovery of inhibited MMP-9 expression.