miR-145-5p promotes trophoblast cell growth and invasion by targeting FLT1.

Abstract:

OBJECTIVE:We aimed to explore the expression level and biological function of miR-145-5p in preeclampsia (PE). METHODS:The differentially expressed miRNA/mRNA between normal placentas and PE placentas were screened using the GSE84260 and GSE73374 datasets from the Gene Expression Omnibus Database. The expression of miR-145-5p in PE placentas was detected by qRT-PCR. The CCK-8 assay, wound healing and transwell were carried out to determine the cell growth, migration and invasion when miR-145-5p was overexpressed or inhibited. The real-time quantitative PCR (qRT-PCR), Western Blot and dual-luciferase reporter assays were conducted to preliminarily explore possible mechanisms. RESULTS:A total of 33 miRNAs were found significantly differentially expressed in PE patients, 19 were significantly upregulated and 14 were significantly downregulated. The relative miR-145-5p expression was lower in PE placentas than normal placentas. The viability and invasion were suppressed when miR-145-5p was inhibited in trophoblasts cells, while miR-145-5p overexpression promoted the effectiveness. In addition, mRNA and protein expression of FLT1 in HTR-8/SVneo cell was also downregulated with miR-145-5p overexpression, suggesting that FLT1 is the target gene of miR-145-5p. Consistent with miR-145-5p overexpression, the mRNA and protein expression of FLT1 also were upregulated with miR-145-5p interference. Furthermore, the expression of miR-145-5p was regulated by the Hypoxic conditions. CONCLUSIONS:In conclusion, the results showed miR-145-5p may participate in PE development by affecting the proliferation and invasion of trophoblast cells. This is a new perspective to understand the etiology and pathogenesis of PE, which may provide a new breakthrough for the early prediction and diagnosis of PE.

journal_name

Life Sci

journal_title

Life sciences

authors

Lv Y,Lu X,Li C,Fan Y,Ji X,Long W,Meng L,Wu L,Wang L,Lv M,Ding H

doi

10.1016/j.lfs.2019.117008

subject

Has Abstract

pub_date

2019-12-15 00:00:00

pages

117008

eissn

0024-3205

issn

1879-0631

pii

S0024-3205(19)30935-X

journal_volume

239

pub_type

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