Min Zhang1, Ping Li1, Xuemei Mao1, Hongyan Zhang2. 1. Department of Obstetrics, Tianjin NanKai Hospital, Tianjin, China. 2. Department of Gynecology, Nankai District Hospital of Traditional Chinese Medicine, Tianjin, China.
Abstract
AIM: To investigate the mechanism of miRNA-525-5p (miR-525-5p) in regulating the invasion of trophoblast cells. METHODS: The expressions of miR-525-5p and Homeobox D10 (HOXD10) in pre-eclampsia (PE) and normal placentas were detected. Besides the expressions of miR-525-5p and HOXD10, the levels of Vimentin, N-cadherin and E-cadherin in human trophoblast (HTR)-8 cells were also measured after cell transfection. 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT) and Transwell assays assessed the proliferative and invasive capabilities of HTR-8 cells, respectively. Dual-luciferase reporter assay verified the targeting relationship between miR-525-5p and HOXD10. RESULTS: MiR-525-5p was lowly expressed and HOXD10 was highly expressed in PE placentas. MiR-525-5p inhibition or HOXD10 overexpression suppressed proliferation, invasion and epithelial-mesenchymal transition (EMT) of HTR-8 cells. MiR-525-5p overexpression or HOXD10 knockdown promoted proliferation, invasion and EMT of HTR-8 cells. HOXD10 was a downstream target of miR-525-5p. Inhibiting HOXD10 reversed the suppressive effects of miR-525-5p inhibition on proliferation, invasion and EMT of HTR-8 cells. CONCLUSION: MiR-525-5p mediates the invasion of trophoblast cells by regulating HOXD10, which provides new therapeutic targets for PE treatment.
AIM: To investigate the mechanism of miRNA-525-5p (miR-525-5p) in regulating the invasion of trophoblast cells. METHODS: The expressions of miR-525-5p and Homeobox D10 (HOXD10) in pre-eclampsia (PE) and normal placentas were detected. Besides the expressions of miR-525-5p and HOXD10, the levels of Vimentin, N-cadherin and E-cadherin in human trophoblast (HTR)-8 cells were also measured after cell transfection. 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT) and Transwell assays assessed the proliferative and invasive capabilities of HTR-8 cells, respectively. Dual-luciferase reporter assay verified the targeting relationship between miR-525-5p and HOXD10. RESULTS: MiR-525-5p was lowly expressed and HOXD10 was highly expressed in PE placentas. MiR-525-5p inhibition or HOXD10 overexpression suppressed proliferation, invasion and epithelial-mesenchymal transition (EMT) of HTR-8 cells. MiR-525-5p overexpression or HOXD10 knockdown promoted proliferation, invasion and EMT of HTR-8 cells. HOXD10 was a downstream target of miR-525-5p. Inhibiting HOXD10 reversed the suppressive effects of miR-525-5p inhibition on proliferation, invasion and EMT of HTR-8 cells. CONCLUSION: MiR-525-5p mediates the invasion of trophoblast cells by regulating HOXD10, which provides new therapeutic targets for PE treatment.