FGD5-AS1 promotes growth and mobility of trophoblast cells by regulating IGF2 via sponging miR-16-5p in pre-eclampsia

Background PE is a common pregnancy disease that can cause various pathologies in pregnant women. GEO microarray data revealed low expression of FGD5-AS1 in placenta tissues from patients with severe PE. As predicted by ENCORI, FGD5-AS1 sponges miR-16-5p, and IGF2, and promotes cell proliferation, differentiation, and metabolism. Objectives This study aimed to interrogate the interaction of FGD5-AS1/miR-16-5p/IGF2 axis and the mechanism of FGD5-AS1 in hypoxia-induced trophoblast cell injury. Results Our findings revealed that FGD5-AS1 and IGF2 were substantially decreased in PE patients than that in normal pregnant females, whereas miR-16-5p was increased in PE patients than that in normal pregnant females. In vitro studies showed that FGD5-AS1 were reduced in trophoblast cells after hypoxia treatment, accompanied by decreased viability and increased apoptosis, also reduced invasion, migration and angiogenesis. However, FGD5-AS1 overexpression substantially reversed these effects. Further mechanistic analysis showed that FGD5-AS1 could target miR-16-5p to regulate IGF2. FGD5-AS1 promoted the expression of IGF2 by sponging miR-16-5p, thereby increasing the viability of trophoblast cells after hypoxia treatment and promoting invasion and migration. Conclusion Overall, our findings demonstrated that FGD5-AS1 promoted growth and mobility of trophoblast cells by regulating miR-16-5p/IGF2 axis in PE.