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Long non-coding RNA HLA-F antisense RNA 1 inhibits the maturation of microRNA-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis

MicroRNA-613 (miR-613) inhibits granulosa cell proliferation, suggesting its involvement in polycystic ovary syndrome (PCOS). We predicted that long non-coding RNA (lncRNA) HLA-F antisense RNA 1 (HLA-F-AS1) could interact with premature miR-613. We then explored the crosstalk between HLA-F-AS1 and m...

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Autores principales: Li, Xiaohua, Zhu, Laifang, Luo, Yan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9275988/
https://www.ncbi.nlm.nih.gov/pubmed/35603775
http://dx.doi.org/10.1080/21655979.2022.2070965
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author Li, Xiaohua
Zhu, Laifang
Luo, Yan
author_facet Li, Xiaohua
Zhu, Laifang
Luo, Yan
author_sort Li, Xiaohua
collection PubMed
description MicroRNA-613 (miR-613) inhibits granulosa cell proliferation, suggesting its involvement in polycystic ovary syndrome (PCOS). We predicted that long non-coding RNA (lncRNA) HLA-F antisense RNA 1 (HLA-F-AS1) could interact with premature miR-613. We then explored the crosstalk between HLA-F-AS1 and miR-613 in PCOS. In this study, follicular fluid donated by 58 healthy controls and 58 PCOS patients was used to analyze the expression of HLA-F-AS1 and miR-613 (mature and premature). The direct interaction between HLA-F-AS1 and premature miR-613 was evaluated by RNA pull-down assay. Overexpression of both HLA-F-AS1 and miR-613 was achieved in granulosa cells to assess their interactions. Cell proliferation and apoptosis were detected with BrdU assay and cell apoptosis assay, respectively. We found that miR-613 was highly expressed in PCOS, while HLA-F-AS1 was downregulated in PCOS. HLA-F-AS1 directly interacted with premature miR-613, and overexpression of HLA-F-AS1 increased the expression levels of premature miR-613, but decreased the expression levels of mature miR-613. HLA-F-AS1 increased ovarian granulosa cell proliferation and inhibited cell apoptosis. MiR-613 played an opposite role and suppressed the role of HLA-F-AS1. Therefore, HLA-F-AS1 may inhibit the maturation of miR-613 in PCOS to promote ovarian granulosa cell proliferation and inhibit cell apoptosis.
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spelling pubmed-92759882022-07-13 Long non-coding RNA HLA-F antisense RNA 1 inhibits the maturation of microRNA-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis Li, Xiaohua Zhu, Laifang Luo, Yan Bioengineered Research Paper MicroRNA-613 (miR-613) inhibits granulosa cell proliferation, suggesting its involvement in polycystic ovary syndrome (PCOS). We predicted that long non-coding RNA (lncRNA) HLA-F antisense RNA 1 (HLA-F-AS1) could interact with premature miR-613. We then explored the crosstalk between HLA-F-AS1 and miR-613 in PCOS. In this study, follicular fluid donated by 58 healthy controls and 58 PCOS patients was used to analyze the expression of HLA-F-AS1 and miR-613 (mature and premature). The direct interaction between HLA-F-AS1 and premature miR-613 was evaluated by RNA pull-down assay. Overexpression of both HLA-F-AS1 and miR-613 was achieved in granulosa cells to assess their interactions. Cell proliferation and apoptosis were detected with BrdU assay and cell apoptosis assay, respectively. We found that miR-613 was highly expressed in PCOS, while HLA-F-AS1 was downregulated in PCOS. HLA-F-AS1 directly interacted with premature miR-613, and overexpression of HLA-F-AS1 increased the expression levels of premature miR-613, but decreased the expression levels of mature miR-613. HLA-F-AS1 increased ovarian granulosa cell proliferation and inhibited cell apoptosis. MiR-613 played an opposite role and suppressed the role of HLA-F-AS1. Therefore, HLA-F-AS1 may inhibit the maturation of miR-613 in PCOS to promote ovarian granulosa cell proliferation and inhibit cell apoptosis. Taylor & Francis 2022-05-21 /pmc/articles/PMC9275988/ /pubmed/35603775 http://dx.doi.org/10.1080/21655979.2022.2070965 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Li, Xiaohua
Zhu, Laifang
Luo, Yan
Long non-coding RNA HLA-F antisense RNA 1 inhibits the maturation of microRNA-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis
title Long non-coding RNA HLA-F antisense RNA 1 inhibits the maturation of microRNA-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis
title_full Long non-coding RNA HLA-F antisense RNA 1 inhibits the maturation of microRNA-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis
title_fullStr Long non-coding RNA HLA-F antisense RNA 1 inhibits the maturation of microRNA-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis
title_full_unstemmed Long non-coding RNA HLA-F antisense RNA 1 inhibits the maturation of microRNA-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis
title_short Long non-coding RNA HLA-F antisense RNA 1 inhibits the maturation of microRNA-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis
title_sort long non-coding rna hla-f antisense rna 1 inhibits the maturation of microrna-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9275988/
https://www.ncbi.nlm.nih.gov/pubmed/35603775
http://dx.doi.org/10.1080/21655979.2022.2070965
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