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Long non-coding RNA placenta‑specific protein 2 regulates micorRNA-19a/tumor necrosis factor α to participate in polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is a type of hormonal disorder that affects about 5–20% of females at their reproductive age worldwide. MicorRNA-19a (miR-19a) is a well-characterized miRNA in cancer biology and its function is mainly mediated by targeting tumor necrosis factor α (TNF-α), which play...

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Autores principales: Li, Gang, Wang, Yongli, Wang, Jingyuan, Chen, Gong, Wang, Haiyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8805902/
https://www.ncbi.nlm.nih.gov/pubmed/34967266
http://dx.doi.org/10.1080/21655979.2021.2013722
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author Li, Gang
Wang, Yongli
Wang, Jingyuan
Chen, Gong
Wang, Haiyan
author_facet Li, Gang
Wang, Yongli
Wang, Jingyuan
Chen, Gong
Wang, Haiyan
author_sort Li, Gang
collection PubMed
description Polycystic ovary syndrome (PCOS) is a type of hormonal disorder that affects about 5–20% of females at their reproductive age worldwide. MicorRNA-19a (miR-19a) is a well-characterized miRNA in cancer biology and its function is mainly mediated by targeting tumor necrosis factor α (TNF-α), which plays critical roles in PCOS. Our preliminary analysis predicted the potential interaction between miR-19a and long non-coding RNA (lncRNA) placenta‑specific protein 2 (PLAC2). Therefore, this study aimed to explore the role of PLAC2 in PCOS. Ovarian tissues were collected from 62 PCOS patients and 62 healthy females. Granulosa-like tumor cells (KGN) was prepared, and transient transfections was conducted. Dual-luciferase activity assay was used to investigate the interaction between PLAC2 and miR-19a. qPCR assays were performed for the expression analysis of miR-19a/TNF-α. In addition, Western blot analysis and cell apoptosis assay were conducted. The results showed that PLAC2 was upregulated in PCOS. PLAC2 and miR-19a showed a direct interaction, while overexpression of PLAC2 and miR-19a did not affect the expression of each other in KGN cells. Instead, overexpression of PLAC2 led to upregulated TNF-α, which is a target of miR-19a. Cell apoptosis analysis showed that PLAC2 and TNF-α promoted the apoptosis of KGN cells. Overexpression of miR-19a played an opposite role. In addition, the overexpression of PLAC2 reduced the effects of overexpression of miR-19a. Therefore, PLAC2 may regulate miR-19a/TNF-α to participate in PCOS.
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spelling pubmed-88059022022-02-02 Long non-coding RNA placenta‑specific protein 2 regulates micorRNA-19a/tumor necrosis factor α to participate in polycystic ovary syndrome Li, Gang Wang, Yongli Wang, Jingyuan Chen, Gong Wang, Haiyan Bioengineered Research Paper Polycystic ovary syndrome (PCOS) is a type of hormonal disorder that affects about 5–20% of females at their reproductive age worldwide. MicorRNA-19a (miR-19a) is a well-characterized miRNA in cancer biology and its function is mainly mediated by targeting tumor necrosis factor α (TNF-α), which plays critical roles in PCOS. Our preliminary analysis predicted the potential interaction between miR-19a and long non-coding RNA (lncRNA) placenta‑specific protein 2 (PLAC2). Therefore, this study aimed to explore the role of PLAC2 in PCOS. Ovarian tissues were collected from 62 PCOS patients and 62 healthy females. Granulosa-like tumor cells (KGN) was prepared, and transient transfections was conducted. Dual-luciferase activity assay was used to investigate the interaction between PLAC2 and miR-19a. qPCR assays were performed for the expression analysis of miR-19a/TNF-α. In addition, Western blot analysis and cell apoptosis assay were conducted. The results showed that PLAC2 was upregulated in PCOS. PLAC2 and miR-19a showed a direct interaction, while overexpression of PLAC2 and miR-19a did not affect the expression of each other in KGN cells. Instead, overexpression of PLAC2 led to upregulated TNF-α, which is a target of miR-19a. Cell apoptosis analysis showed that PLAC2 and TNF-α promoted the apoptosis of KGN cells. Overexpression of miR-19a played an opposite role. In addition, the overexpression of PLAC2 reduced the effects of overexpression of miR-19a. Therefore, PLAC2 may regulate miR-19a/TNF-α to participate in PCOS. Taylor & Francis 2021-12-30 /pmc/articles/PMC8805902/ /pubmed/34967266 http://dx.doi.org/10.1080/21655979.2021.2013722 Text en © 2021 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, Gang
Wang, Yongli
Wang, Jingyuan
Chen, Gong
Wang, Haiyan
Long non-coding RNA placenta‑specific protein 2 regulates micorRNA-19a/tumor necrosis factor α to participate in polycystic ovary syndrome
title Long non-coding RNA placenta‑specific protein 2 regulates micorRNA-19a/tumor necrosis factor α to participate in polycystic ovary syndrome
title_full Long non-coding RNA placenta‑specific protein 2 regulates micorRNA-19a/tumor necrosis factor α to participate in polycystic ovary syndrome
title_fullStr Long non-coding RNA placenta‑specific protein 2 regulates micorRNA-19a/tumor necrosis factor α to participate in polycystic ovary syndrome
title_full_unstemmed Long non-coding RNA placenta‑specific protein 2 regulates micorRNA-19a/tumor necrosis factor α to participate in polycystic ovary syndrome
title_short Long non-coding RNA placenta‑specific protein 2 regulates micorRNA-19a/tumor necrosis factor α to participate in polycystic ovary syndrome
title_sort long non-coding rna placenta‑specific protein 2 regulates micorrna-19a/tumor necrosis factor α to participate in polycystic ovary syndrome
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8805902/
https://www.ncbi.nlm.nih.gov/pubmed/34967266
http://dx.doi.org/10.1080/21655979.2021.2013722
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