MALAT1 modulates trophoblast phenotype via miR-101-3p/VEGFA axis

Arch Biochem Biophys. 2023 Jul 10:109692. doi: 10.1016/j.abb.2023.109692. Online ahead of print.ABSTRACTPreeclampsia is a potentially life-threatening condition that can arise due to poor placentation and consequent abnormal uterine spiral artery remodeling. Abnormal placentation, in turn, is associated with aberrant trophoblast cell proliferation and apoptosis. Here, we investigated the lncRNA MALAT1 in trophoblast proliferation during early-onset preeclampsia (ePE). MALAT1 levels were examined in placental tissue samples from ePE patients and control patients. The effects and underlying mechanism of MALAT1 on proliferation, migration, invasion and apoptosis were investigated in the first-trimester extravillous trophoblast HTR-8/SVneo cells and the human choriocarcinoma JAR cells. MALAT1 levels were decreased in the placental tissue samples of ePE patients compared with those of control patients, and the levels of MALAT1 were positively correlated with the neonate birth-weight. Knockdown of MALAT1 attenuated the cell viability, proliferation, migration, invasion and the cell cycle progression of trophoblasts, but promoted the apoptosis of trophoblasts. The MALAT1 knockdown promoted miR-101-3p upregulation and VEGFA downregulation. Inhibitor of miR-101-3p increased vascular endothelial growth factor A (VEGFA) expression, and miR-101-3p mimic inhibited VEGFA expression. Luciferase assays showed that miR-101-3p could bind to both MALAT1 and VEGFA. The MALAT1 knockdown-induced i...
Source: Archives of Biochemistry and Biophysics - Category: Biochemistry Authors: Source Type: research