Highly expressed FYN promotes the progression of placenta accreta by activating STAT3, p38, and JNK signaling pathways

Abstract

Placenta accreta is an abnormality of the placenta caused by the chorionic villi invading the muscular layer, which can cause serious bleeding, infection, shock, bladder invasion, uterine perforation, and even death. However, the etiology of placental accreta is not entirely clear. In the present study, high-throughput sequencing results showed that FYN is highly expressed in the placental accreta position in the placenta accreta group and is a key regulator of cell invasion and migration. Therefore, we aimed to evaluate the role and potential molecular mechanism of FYN in placenta accreta. The results showed that FYN was highly expressed in the placenta tissues of the placenta accreta group. Furthermore, the levels of phosphorylated STAT3, p38, and JNK in the placenta accreta group were remarkably increased compared with those in the control group. In addition, FYN knockdown considerably decreased the migration and invasion rates of trophoblast cells (HTR8/SVneo) and inhibited the levels of phosphorylated STAT3, p38, and JNK. After subsequently blocking these signaling pathways, the invasion and migration abilities of HTR8/SVneo cells were substantially decreased. In conclusion, FYN may promote excessive trophocyte cell invasion by activating STAT3, p38, and JNK pathways and can be a new target for placenta accreta prevention and treatment.

Keywords: Cell migration and invasion; FYN; Pathogenesis; Placenta accreta; Signaling pathways.