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miR-222 Suppresses Immature Porcine Sertoli Cell Growth by Targeting the GRB10 Gene Through Inactivating the PI3K/AKT Signaling Pathway
Sertoli cells are central and essential coordinators of spermatogenesis. Accumulating evidence has demonstrated that miRNAs participate in the regulation of Sertoli cell growth. However, the functions and the regulatory mechanisms of miRNAs in Sertoli cells of domestic animals remain largely unknown...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673446/ https://www.ncbi.nlm.nih.gov/pubmed/33329720 http://dx.doi.org/10.3389/fgene.2020.581593 |
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author | Luo, Hui Peng, Fuzhi Weng, Bo Tang, Xiangwei Chen, Yao Yang, Anqi Chen, Bin Ran, Maoliang |
author_facet | Luo, Hui Peng, Fuzhi Weng, Bo Tang, Xiangwei Chen, Yao Yang, Anqi Chen, Bin Ran, Maoliang |
author_sort | Luo, Hui |
collection | PubMed |
description | Sertoli cells are central and essential coordinators of spermatogenesis. Accumulating evidence has demonstrated that miRNAs participate in the regulation of Sertoli cell growth. However, the functions and the regulatory mechanisms of miRNAs in Sertoli cells of domestic animals remain largely unknown. Here we report that miR-222 overexpression repressed cell cycle progression and proliferation and promoted the apoptosis of immature porcine Sertoli cells, whereas miR-222 inhibition resulted in the opposite result. miR-222 directly targeted the 3′-UTR of the GRB10 gene and inhibited its mRNA abundance. An siRNA-induced GRB10 knockdown showed similar effects as did miR-222 overexpression on cell proliferation and apoptosis and further attenuated the role of miR-222 inhibition. Furthermore, both miR-222 overexpression and GRB10 inhibition repressed the phosphorylation of PI3K and AKT, the key elements of the PI3K/AKT signaling pathway, whereas GRB10 inhibition offsets the effects of the miR-222 knockdown. Overall, we concluded that miR-222 suppresses immature porcine Sertoli cell growth by targeting the GRB10 gene through inactivation of the PI3K/AKT signaling pathway. This study provides novel insights into the epigenetic regulation of porcine spermatogenesis by determining the fate of Sertoli cells. |
format | Online Article Text |
id | pubmed-7673446 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-76734462020-12-15 miR-222 Suppresses Immature Porcine Sertoli Cell Growth by Targeting the GRB10 Gene Through Inactivating the PI3K/AKT Signaling Pathway Luo, Hui Peng, Fuzhi Weng, Bo Tang, Xiangwei Chen, Yao Yang, Anqi Chen, Bin Ran, Maoliang Front Genet Genetics Sertoli cells are central and essential coordinators of spermatogenesis. Accumulating evidence has demonstrated that miRNAs participate in the regulation of Sertoli cell growth. However, the functions and the regulatory mechanisms of miRNAs in Sertoli cells of domestic animals remain largely unknown. Here we report that miR-222 overexpression repressed cell cycle progression and proliferation and promoted the apoptosis of immature porcine Sertoli cells, whereas miR-222 inhibition resulted in the opposite result. miR-222 directly targeted the 3′-UTR of the GRB10 gene and inhibited its mRNA abundance. An siRNA-induced GRB10 knockdown showed similar effects as did miR-222 overexpression on cell proliferation and apoptosis and further attenuated the role of miR-222 inhibition. Furthermore, both miR-222 overexpression and GRB10 inhibition repressed the phosphorylation of PI3K and AKT, the key elements of the PI3K/AKT signaling pathway, whereas GRB10 inhibition offsets the effects of the miR-222 knockdown. Overall, we concluded that miR-222 suppresses immature porcine Sertoli cell growth by targeting the GRB10 gene through inactivation of the PI3K/AKT signaling pathway. This study provides novel insights into the epigenetic regulation of porcine spermatogenesis by determining the fate of Sertoli cells. Frontiers Media S.A. 2020-10-29 /pmc/articles/PMC7673446/ /pubmed/33329720 http://dx.doi.org/10.3389/fgene.2020.581593 Text en Copyright © 2020 Luo, Peng, Weng, Tang, Chen, Yang, Chen and Ran. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Genetics Luo, Hui Peng, Fuzhi Weng, Bo Tang, Xiangwei Chen, Yao Yang, Anqi Chen, Bin Ran, Maoliang miR-222 Suppresses Immature Porcine Sertoli Cell Growth by Targeting the GRB10 Gene Through Inactivating the PI3K/AKT Signaling Pathway |
title | miR-222 Suppresses Immature Porcine Sertoli Cell Growth by Targeting the GRB10 Gene Through Inactivating the PI3K/AKT Signaling Pathway |
title_full | miR-222 Suppresses Immature Porcine Sertoli Cell Growth by Targeting the GRB10 Gene Through Inactivating the PI3K/AKT Signaling Pathway |
title_fullStr | miR-222 Suppresses Immature Porcine Sertoli Cell Growth by Targeting the GRB10 Gene Through Inactivating the PI3K/AKT Signaling Pathway |
title_full_unstemmed | miR-222 Suppresses Immature Porcine Sertoli Cell Growth by Targeting the GRB10 Gene Through Inactivating the PI3K/AKT Signaling Pathway |
title_short | miR-222 Suppresses Immature Porcine Sertoli Cell Growth by Targeting the GRB10 Gene Through Inactivating the PI3K/AKT Signaling Pathway |
title_sort | mir-222 suppresses immature porcine sertoli cell growth by targeting the grb10 gene through inactivating the pi3k/akt signaling pathway |
topic | Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673446/ https://www.ncbi.nlm.nih.gov/pubmed/33329720 http://dx.doi.org/10.3389/fgene.2020.581593 |
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