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Regulatory mechanism of miR ‐525‐5p in over‐invasion of trophoblast
Author(s) -
Zhang Min,
Li Ping,
Mao Xuemei,
Zhang Hongyan
Publication year - 2021
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/jog.14581
Subject(s) - trophoblast , vimentin , gene knockdown , transfection , cancer research , epithelial–mesenchymal transition , microrna , cell growth , biology , microbiology and biotechnology , downregulation and upregulation , cell culture , placenta , immunology , immunohistochemistry , biochemistry , fetus , gene , pregnancy , genetics
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.