MiR-507 inhibits the growth and invasion of trophoblasts by targeting CAMK4

To elucidate the potential influences of miR-507 and CAMK4 on the progression of preeclampsia (PE).

Placental tissues were collected from 24 PE pregnancies and 24 healthy pregnancies. The relative levels of miR-507 and CAMK4 in placental tissues were detected. In addition, expressions of apoptosis-associated genes in collected tissues were examined by both quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). The influences of miR-507 and CAMK4 on proliferative and migratory abilities in HTR-8/SVneo cells were assessed by CCK-8 and transwell assay, respectively. The target relationship between miR-507 and CAMK4 was detected by Luciferase assay.

MiR-507 was upregulated in placental tissues collected from PE pregnancies. Overexpression of miR-507 suppressed proliferative and migratory abilities, and stimulated apoptosis in HTR-8/SVneo cells. CAMK4 was the target gene of miR-507, which was downregulated in placental tissues collected from PE pregnancies and negatively correlated to miR-507 level. The knockdown of CAMK4 suppressed proliferative and migratory abilities, and stimulated apoptosis in HTR-8/SVneo cells, and these trends were abolished by silence of miR-507.

Highly expressed miR-507 in PE pregnancies inhibits proliferative and migratory potentials, and induces apoptosis in trophoblasts by targeting CAMK4.