Circular RNA FOXP1 relieves trophoblastic cell dysfunction in recurrent pregnancy loss via the miR-143-3p/S100A11 cascade

Recurrent pregnancy loss (RPL) is closely associated with insufficient functions of trophoblastic cells. Circular RNA forkhead box P1 (circFOXP1) can regulate cell activities in different types of diseases. However, its effects on trophoblastic cells and its role in RPL development remain unknown. I...

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Autores principales: Yuan Gao, Yukun Tang, Qian Sun, Guixue Guan, Xiaoyan Wu, Fan Shi, Zihao Zhou, Wen Yang
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Publicado: Taylor & Francis Group 2021
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spelling oai:doaj.org-article:2195b49076a2444497ced6d650d3025c2021-11-04T15:51:53ZCircular RNA FOXP1 relieves trophoblastic cell dysfunction in recurrent pregnancy loss via the miR-143-3p/S100A11 cascade2165-59792165-598710.1080/21655979.2021.1988374https://doaj.org/article/2195b49076a2444497ced6d650d3025c2021-01-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1988374https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Recurrent pregnancy loss (RPL) is closely associated with insufficient functions of trophoblastic cells. Circular RNA forkhead box P1 (circFOXP1) can regulate cell activities in different types of diseases. However, its effects on trophoblastic cells and its role in RPL development remain unknown. In this study, gene expressions were detected by RT-qPCR. Protein levels were detected by Western blotting. Trophoblastic cell viability, apoptosis, invasion, and migration were respectively analyzed via CCK-8, flow cytometry, wound healing, and transwell assays. The association between miR–143–3p and circFOXP1 or S100A11 (S100 calcium binding protein A11) was explored and confirmed by bioinformatics prediction and luciferase reporter assay. Herein, miR–143–3p was upregulated in RPL. Furthermore, miR–143–3p upregulation induced apoptosis and suppressed proliferation, epithelial-to-mesenchymal transition (EMT) process, and metastatic capabilities of trophoblastic cells; whereas, miR–143–3p inhibition exert opposite effects. MiR–143–3p targeted S100A11 and was adversely regulated by circFOXP1 expression. S100A11 inhibition partially offset the effect of miR–143–3p knockdown on trophoblastic cell viability, apoptosis, EMT, invasion, and migration. In addition, circFOXP1 competitively combined with miR–143–3p, thus regulating S100A11 expression. Moreover, circFOXP1 regulated trophoblastic cell functions through the miR–143–3p/S100A11 cascade. To sum up, our study, for the first time, demonstrated that circFOXP1 could improve dysfunction of trophoblastic cells through the miR–143–3p/S100A11 axis, providing novel biomarkers and diagnostic targets for RPL.Yuan GaoYukun TangQian SunGuixue GuanXiaoyan WuFan ShiZihao ZhouWen YangTaylor & Francis Grouparticlecircfoxp1mir–143–3ps100a11recurrent pregnancy lossepithelial-to-mesenchymal transitionBiotechnologyTP248.13-248.65ENBioengineered, Vol 12, Iss 1, Pp 9081-9093 (2021)
institution DOAJ
collection DOAJ
language EN
topic circfoxp1
mir–143–3p
s100a11
recurrent pregnancy loss
epithelial-to-mesenchymal transition
Biotechnology
TP248.13-248.65
spellingShingle circfoxp1
mir–143–3p
s100a11
recurrent pregnancy loss
epithelial-to-mesenchymal transition
Biotechnology
TP248.13-248.65
Yuan Gao
Yukun Tang
Qian Sun
Guixue Guan
Xiaoyan Wu
Fan Shi
Zihao Zhou
Wen Yang
Circular RNA FOXP1 relieves trophoblastic cell dysfunction in recurrent pregnancy loss via the miR-143-3p/S100A11 cascade
description Recurrent pregnancy loss (RPL) is closely associated with insufficient functions of trophoblastic cells. Circular RNA forkhead box P1 (circFOXP1) can regulate cell activities in different types of diseases. However, its effects on trophoblastic cells and its role in RPL development remain unknown. In this study, gene expressions were detected by RT-qPCR. Protein levels were detected by Western blotting. Trophoblastic cell viability, apoptosis, invasion, and migration were respectively analyzed via CCK-8, flow cytometry, wound healing, and transwell assays. The association between miR–143–3p and circFOXP1 or S100A11 (S100 calcium binding protein A11) was explored and confirmed by bioinformatics prediction and luciferase reporter assay. Herein, miR–143–3p was upregulated in RPL. Furthermore, miR–143–3p upregulation induced apoptosis and suppressed proliferation, epithelial-to-mesenchymal transition (EMT) process, and metastatic capabilities of trophoblastic cells; whereas, miR–143–3p inhibition exert opposite effects. MiR–143–3p targeted S100A11 and was adversely regulated by circFOXP1 expression. S100A11 inhibition partially offset the effect of miR–143–3p knockdown on trophoblastic cell viability, apoptosis, EMT, invasion, and migration. In addition, circFOXP1 competitively combined with miR–143–3p, thus regulating S100A11 expression. Moreover, circFOXP1 regulated trophoblastic cell functions through the miR–143–3p/S100A11 cascade. To sum up, our study, for the first time, demonstrated that circFOXP1 could improve dysfunction of trophoblastic cells through the miR–143–3p/S100A11 axis, providing novel biomarkers and diagnostic targets for RPL.
format article
author Yuan Gao
Yukun Tang
Qian Sun
Guixue Guan
Xiaoyan Wu
Fan Shi
Zihao Zhou
Wen Yang
author_facet Yuan Gao
Yukun Tang
Qian Sun
Guixue Guan
Xiaoyan Wu
Fan Shi
Zihao Zhou
Wen Yang
author_sort Yuan Gao
title Circular RNA FOXP1 relieves trophoblastic cell dysfunction in recurrent pregnancy loss via the miR-143-3p/S100A11 cascade
title_short Circular RNA FOXP1 relieves trophoblastic cell dysfunction in recurrent pregnancy loss via the miR-143-3p/S100A11 cascade
title_full Circular RNA FOXP1 relieves trophoblastic cell dysfunction in recurrent pregnancy loss via the miR-143-3p/S100A11 cascade
title_fullStr Circular RNA FOXP1 relieves trophoblastic cell dysfunction in recurrent pregnancy loss via the miR-143-3p/S100A11 cascade
title_full_unstemmed Circular RNA FOXP1 relieves trophoblastic cell dysfunction in recurrent pregnancy loss via the miR-143-3p/S100A11 cascade
title_sort circular rna foxp1 relieves trophoblastic cell dysfunction in recurrent pregnancy loss via the mir-143-3p/s100a11 cascade
publisher Taylor & Francis Group
publishDate 2021
url https://doaj.org/article/2195b49076a2444497ced6d650d3025c
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