Silencing BRIT1 Facilitates the Abilities of Invasiveness and Migration in Trophoblast Cells

Liu, Luping; Sun, Li; Zheng, Jing; Wang, Yanchun

doi:10.12659/msm.910229

Cited by 3 publications

(3 citation statements)

References 43 publications

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“…Xing et al found that knockdown of WNT3 expression in tumor cells significantly blocked cell proliferation, delayed cell cycle progression, and suppressed cell invasion and metastasis, accompanied by increased apoptosis [ 31 ]. In addition, increasing the expression of WNT3 accelerated the invasion and migration of trophoblast cells [ 40 ]. The results of this study revealed high expression of WNT3.…”

Section: Discussionmentioning

confidence: 99%

WNT3 hypomethylation counteracts low activity of the Wnt signaling pathway in the placenta of preeclampsia

Zhang

Sang

et al. 2021

Cell. Mol. Life Sci.

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Preeclampsia is a hypertensive disorder of pregnancy. Many studies have shown that epigenetic mechanisms may play a role in preeclampsia. Moreover, our previous study indicated that the differentially methylated genes in preeclampsia were enriched in the Wnt/β-catenin signaling pathway. This study aimed to identify differentially methylated Wnt/β-catenin signaling pathway genes in the preeclamptic placenta and to study the roles of these genes in trophoblast cells in vitro. Using an Illumina Infinium HumanMethylation 850 K BeadChip, we found that the Wnt signaling pathway was globally hypermethylated in the preeclamptic group compared with the term birth group, but hypomethylated in the preeclamptic group compared with the preterm birth group. Among all Wnt/β-catenin signaling pathway factors, WNT3 was the most significantly differentially expressed gene and was hypomethylated in the preeclamptic group compared to the nonhypertensive groups, namely, the preterm birth group and term birth group. This result was confirmed by pyrosequencing. Through quantitative real-time PCR and western blot analysis, the WNT3 gene was found to be highly expressed in preeclamptic placental tissues, in contrast to other WNT factors, which were previously reported to be expressed at low levels in placental tissues. Additionally, in the HTR8/SVneo cell line, knockdown of WNT3 suppressed the Wnt/β-catenin signaling pathway, consistent with the findings for other WNT factors. These results prompted us to speculate that the WNT3 gene counteracts the low activation state of the Wnt signaling pathway in the preeclamptic placenta through methylation modification.

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Section: Discussionmentioning

confidence: 99%

WNT3 hypomethylation counteracts low activity of the Wnt signaling pathway in the placenta of preeclampsia

Zhang

Sang

et al. 2021

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

show abstract

“…Xing Z et al found that knockdown of WNT3 expression in tumor cells signi cantly blocked cell proliferation, delayed cell cycle progression and suppressed cell invasion and metastasis, accompanied by increased apoptosis [31]. In addition, increasing the expression of WNT3 accelerated the invasion and migration of trophoblast cells [40]. The results of this study revealed high expression of WNT3.…”

Section: Discussionmentioning

confidence: 50%

WNT3 Hypopethylation Counteracts low Activity of the Wnt Signaling Pathway in the Placenta of Preeclampsia

Zhang

Sang

et al. 2021

Preprint

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Preeclampsia is a hypertensive disorder of pregnancy. Many studies have shown that epigenetic mechanisms may play a role in preeclampsia. Moreover, our previous study indicated that the differentially methylated genes in preeclampsia were enriched in the Wnt/β-catenin signaling pathway. This study aimed to identify differentially methylated Wnt/β-catenin signaling pathway genes in the preeclamptic placenta and to study the roles of these genes in trophoblast cells in vitro. Using an Illumina Infinium HumanMethylation 850K BeadChip, we found that the Wnt signaling pathway was globally hypermethylated in the preeclamptic group compared with the term birth group but hypomethylated in the preeclamptic group compared with the preterm birth group. Among all Wnt/β-catenin signaling pathway factors, WNT3 was the most significantly differentially expressed gene and was hypomethylated in the preeclamptic group compared to the nonhypertensive groups, namely, the preterm birth group and term birth group. This result was confirmed by pyrosequencing. Through quantitative real-time PCR and western blot analysis, the WNT3 gene was found to be highly expressed in preeclamptic placental tissues, in contrast to other WNT factors, which were previously reported to be expressed at low levels in placental tissues. Additionally, in the HTR8/SVneo cell line, knockdown of WNT3 suppressed the Wnt/β-catenin signaling pathway, consistent with the findings for other WNT factors. These results prompted us to speculate that the WNT3 gene counteracts the low activation state of the Wnt signaling pathway in the preeclamptic placenta through methylation modification.

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“…There are increasing evidences indicate that Wnt/β‐catenin is closely related to the transfer and invasion of trophoblast cells. For instance, Liu et al 27 . demonstrated that BRIT1 silencing activated the Wnt/β‐catenin pathway and accelerated the invasion and migration of trophoblast cells.…”

Section: Introductionmentioning

confidence: 99%

MiR‐95‐5p involves in the migration and invasion of trophoblast cells by targeting low density lipoprotein receptor‐related protein 6

Xiao

et al. 2020

J of Obstet and Gynaecol

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AimsLow density lipoprotein receptor‐related protein 6 (LRP6) has been demonstrated to control trophoblast cell invasion, but its regulatory gene remains undefined. In this study, microRNA (miR) regulating LRP6 were explored to elucidate the potential mechanism of preeclampsia (PE).MethodsFirstly, the expression of LRP6 in PE tissues was detected by immunohistochemical staining and quantitative real‐time polymerase chain reaction (qRT‐PCR) assay. Prediction software predicted that LRP6 might be the target gene of miR‐95‐5p, and verified by double‐luciferase reporter analysis. qRT‐PCR assay measured the expression of miR‐95‐5p in PE tissues and trophoblast cell lines. Then, we transfected miR‐95‐5p mimic, inhibitor, LRP6, or mimic plus LRP6 into trophoblast cell lines, and analyzed their influences on cell migration and invasion by wound healing and Transwell experiments. The expressions of matrix metalloproteinase (MMP)‐2, MMP‐9 and tissue inhibitors of metalloproteinase (TIMP)‐1 in transfected cells were examined by western blot (WB) analysis.ResultsLRP6 was low‐expressed in PE tissues, while miR‐95‐5p expression was high‐expressed. MiR‐95‐5p negatively regulated the LRP6 expression in trophoblast cells. Both up‐regulated LRP6 and down‐regulated miR‐95‐5p can not only promote the migration and invasion of trophoblast cells, but also raised the expressions of MMP‐2 and MMP‐9 and inhibited the expression of TIMP‐1. The over‐expression of miR‐95‐5p suppressed the metastasis of trophoblast cells and rescued LRP6‐induced increase of MMP‐2 and MMP‐9 and reduction of TIMP‐1.ConclusionMiR‐95‐5p involved in the migration and invasion of trophoblast cells by targeting LRP6, which might be a potential therapeutic target for PE.

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Silencing BRIT1 Facilitates the Abilities of Invasiveness and Migration in Trophoblast Cells

Cited by 3 publications

References 43 publications

WNT3 hypomethylation counteracts low activity of the Wnt signaling pathway in the placenta of preeclampsia

WNT3 hypomethylation counteracts low activity of the Wnt signaling pathway in the placenta of preeclampsia

WNT3 Hypopethylation Counteracts low Activity of the Wnt Signaling Pathway in the Placenta of Preeclampsia

MiR‐95‐5p involves in the migration and invasion of trophoblast cells by targeting low density lipoprotein receptor‐related protein 6

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