Potential role of microRNA-424 in regulating ERRγ to suppress trophoblast proliferation and invasion in fetal growth restriction

Zou, Zhiyong; He, Zhiming; Cai, Jian; Huang, Liwu; Zhu, Hui; Luo, Yang

doi:10.1016/j.placenta.2019.07.001

Cited by 15 publications

(12 citation statements)

References 41 publications

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“…[36][37][38] In addition, previous study indicated that miR-424-5p has a potential effect on the trophoblast biological function, it can inhibit proliferation and invasion of trophoblasts. 20 In our study, the expression of miR-424-5p inhibited cells proliferation, migration, and invasion of trophoblastic cell line HTR-8/SVneo. These findings indicate that increased or decreased expression of miR-424-5p could have impact on regulating the proliferation, migration, and invasion of the EVT cells.…”

Section: Discussionmentioning

confidence: 50%

“…19 It has been reported that miR-424-5p can inhibit the migration and invasion of trophoblast cells. 20 Downregulation of miR-424 in placenta is associated with PE, and changed expression of miR-424 might affect the Wnt signaling pathway. 21 Therefore, this study further explored the relationship between miR-424 and Wnt signaling pathway in PE.…”

Section: Introductionmentioning

confidence: 99%

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Long intergenic noncoding RNA 00473 promoting migration and invasion of trophoblastic cell line HTR‐8/SVneo via regulating miR‐424‐5p‐mediated wnt3a/β‐catenin signaling pathway

Liu¹,

Liu²,

Zhang³

et al. 2021

J of Obstet and Gynaecol

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Background: Preeclampsia (PE) is a serious obstetric complication. Recent studies point out that the functions of long intergenic noncoding RNA 00473 (linc00473), miR-424-5p, and Wnt/β-catenin signaling pathway were involved in the invasion and migration of extravillous trophoblast. Here, we investigated the role and mechanism of linc00473 in HTR-8/SVneo trophoblastic cell line and its role in PE. Method: The expression levels of linc00473 and miR-424-5p in placental tissues and the transfection efficiency of miR-424-5p were detected by quantitative real-time polymerase chain reaction (qRT-PCR). HTR-8/SVneo cell invasion and proliferation were determined by transwell and Cell Counting Kit-8 (CCK-8) assays. The protein expressions of wnt3a, p-GSK3β, GSK3β, active β-catenin, and total β-catenin were detected by Western blot. The apoptosis and migration of HTR-8/SVneo cells were detected by flow cytometry and wound healing assays. The targeting relationships between linc00473, miR-424-5p, and wnt3a were predicted by ENCORI database and TargetScan V7.2 and were determined using dual-luciferase reporter assay.Results: The expression level of linc00473 was low and miR-424-5p was high in placenta of PE patients. Linc00473 can target miR-424-5p, while miR-424-5p target wnt3a. High expression of linc00473 and wnt3a promoted cell proliferation, migration, invasion, and inhibited cell apoptosis. However, miR-424-5p mimic inhibited HTR-8/SVneo cells proliferation, migration, invasion, while promoted cell apoptosis, partially reversed the effect of linc00473, while wnt3a overexpression partially counteracted the effect of miR-424-5p mimic. Conclusion: Linc00473 mediates the regulation of Wnt/β-catenin signaling pathway by miR-424-5p to affect the invasion and migration ability of trophoblastic cell line HTR-8/SVneo. It indicated that linc00473 is involved in PE and could be a therapeutic target.

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Section: Discussionmentioning

confidence: 50%

Section: Introductionmentioning

confidence: 99%

Long intergenic noncoding RNA 00473 promoting migration and invasion of trophoblastic cell line HTR‐8/SVneo via regulating miR‐424‐5p‐mediated wnt3a/β‐catenin signaling pathway

Liu¹,

Liu²,

Zhang³

et al. 2021

J of Obstet and Gynaecol

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“…Reproduction (2021) 161 R45-R60 ESRRG in HTR/8SVneo cells. However, this study did not identify a regulatory relationship between miR-424 and the 3'UTR of ESRRG, thus more in-depth studies of miR-424 are required in the future (Zou et al 2019). miR-377 is more highly expressed in human term placentas compared with first-trimester placentas, and overexpression of miR-377 in the first-trimester placental explants reduced cytotrophoblast proliferation (Farrokhnia et al 2014).…”

Section: R55mentioning

confidence: 83%

“…Several other miRNAs have been implicated in placental dysfunction by regulating proliferation, invasion, or invasion of trophoblastic-like cell lines, and by reducing ESRRG expression in other cell lines, these include miR-378a-5p, miR-424, miR-377, and miR-204-5p (Eichner et al 2010, Cheng et al 2018, Zou et al 2019. miR-378a-5p inhibits both mRNA and protein levels of ESRRG in the breast cancer cell line, BT-474 (Eichner et al 2010); it also enhances the invasion and migration of HTR8/ SVneo cells and reduces BeWo cell differentiation (Luo et al 2012, Nadeem et al 2014.…”

Section: Other Esrrg Regulatory Mirnasmentioning

confidence: 99%

The potential role of the E SRRG pathway in placental dysfunction

et al. 2021

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Normal placental development and function is of key importance to fetal growth. Conversely aberrations of placental structure and function are evident in pregnancy complications including fetal growth restriction (FGR) and preeclampsia. Although trophoblast turnover and function is altered in these conditions, their underlying aetiologies and pathophysiology remains unclear, which hampers development of therapeutic interventions. Here we review evidence that supports a role for Estrogen Related Receptor-gamma (ERRγ) in the development of placental dysfunction in FGR and preeclampsia. This relationship deserves particular consideration because ERRγ is highly expressed in normal placenta, is reduced in FGR and preeclampsia and its expression is altered by hypoxia, which is thought to result from deficient placentation seen in FGR and preeclampsia. Several studies have also found microRNA or other potential upstream regulators of ERRγ negatively influence trophoblast function which could contribute to placental dysfunction seen in FGR and preeclampsia. Interestingly, microRNAs regulate ERRγ expression in human trophoblast. Thus, if ERRγ is pivotally associated with the abnormal trophoblast turnover and function it may be targeted by microRNAs or other possible upstream regulators in the placenta. This review explores altered expression of ERRγ and upstream regulation of ERRγ-mediated pathways resulting in the trophoblast turnover, placental vascularisation, and placental metabolism underlying placental dysfunctions. This demonstrates that the ERRγ pathway merits further investigation as a potential therapeutic target in FGR and preeclampsia.

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“…So far, more than 700 miRNAs have been mined, and abnormal expression of some miRNAs has been found to lead to multiple complications during pregnancy and trigger a variety of pathologies, for example like FGR, preeclampsia, and gestational diabetes, and it is of great importance in predicting therapeutic strategies and targeted therapy [9][10][11]. Currently reported miRNAs associated with placental dysfunction are miR-424 [12], miR-18a-5p [13], miR-149 [14], miR-133a [15], and miR-98 [16]. For example, Zou et al found that miR-424 could regulate the proliferation and invasion of trophoblast cell lines and mediate the expression of protein ERRγ and HSD17B1, which took part in the development of FGR [12].…”

Section: Introductionmentioning

confidence: 99%

MiR-212-3p promotes proliferation and migration of trophoblast in fetal growth restriction by targeting placental growth factor

Sun

Chu

2021

Bioengineered

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The purpose of this study was to evaluate the function and possible mechanism of miR-212-3p in fetal growth restriction (FGR) and to demonstrate the relationship between miR-212-3p and placental growth factor (PGF). First, we used qRT-PCR to detect the expression of miR-212-3p and PGF in placental tissues of normal delivery (HC group) and FGR, as well as in human trophoblast cell HTR-8/Svneo. The results revealed that miR-212-3p expression was significantly upregulated and PGF was significantly downregulated in placental tissue in the FGR group compared with the HC group. In addition, interference with miR-212-3p expression increased the proliferation, invasion, and migration of HTR-8/SVneo cells and decreased apoptosis of cells. Meanwhile, Western blot results showed that miR-212-3p expression downregulation promoted the phosphorylated protein expression of Phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT), which in turn activated the PI3K/AKT signaling pathway. And the results of dual luciferase reporter further showed that miR-212-3p could target PGF, and the expression of both was negatively correlated in FGR group tissues. In addition, downregulation of miR-212-3p expression reversed the inhibitory effect of PGF downregulation on HTR-8/SVneo cells. In conclusion, miR-212-3p can target and inhibit the PGF expression and regulate the PI3K/AKT signaling pathway to regulate trophoblast cell invasion, migration, proliferation and cell apoptosis. This provides a potential biomarker for the development of FGR.

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Potential role of microRNA-424 in regulating ERRγ to suppress trophoblast proliferation and invasion in fetal growth restriction

Cited by 15 publications

References 41 publications

Long intergenic noncoding RNA 00473 promoting migration and invasion of trophoblastic cell line HTR‐8/SVneo via regulating miR‐424‐5p‐mediated wnt3a/β‐catenin signaling pathway

Long intergenic noncoding RNA 00473 promoting migration and invasion of trophoblastic cell line HTR‐8/SVneo via regulating miR‐424‐5p‐mediated wnt3a/β‐catenin signaling pathway

The potential role of the E SRRG pathway in placental dysfunction

MiR-212-3p promotes proliferation and migration of trophoblast in fetal growth restriction by targeting placental growth factor

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