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

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

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.

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

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