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miR-22-5p regulates the self-renewal of spermatogonial stem cells by targeting EZH2

MiRNAs play an important role in spermatogonial stem cells (SSCs). The purpose of this study was to investigate the basic function of miR-22-5p in cryptorchidism. The results of RT-PCR, western blot, and immunohistochemistry showed that miR-22-5p was increased while EZH2 decreased in the testicular...

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Detalles Bibliográficos
Autores principales: Lv, Wenqiang, Yu, Mei, Su, Yilin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: De Gruyter 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8932390/
https://www.ncbi.nlm.nih.gov/pubmed/35415251
http://dx.doi.org/10.1515/med-2022-0429
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author Lv, Wenqiang
Yu, Mei
Su, Yilin
author_facet Lv, Wenqiang
Yu, Mei
Su, Yilin
author_sort Lv, Wenqiang
collection PubMed
description MiRNAs play an important role in spermatogonial stem cells (SSCs). The purpose of this study was to investigate the basic function of miR-22-5p in cryptorchidism. The results of RT-PCR, western blot, and immunohistochemistry showed that miR-22-5p was increased while EZH2 decreased in the testicular tissues of patients with cryptorchidism. Overexpression of miR-22-5p inhibited the proliferation of SSCs, increased cell apoptosis rate, and reduced expression of SSC marker proteins (GDNF and DAZL); however, knockout of miR-22-5p has the opposite effect. The Luciferase reporter gene assays demonstrated that EZH2 is a direct target of miR-22-5p. Moreover, EZH2 overexpression could reverse the effect of miR-22-5p mimic on SSCs’ proliferation, apoptosis, and expression of SSC marker proteins. Our results demonstrated that miR-22-5p regulates SSCs’ self-renewal by targeting EZH2, which indicated that miR-22-5p may serve as a biological marker for the treatment of infertility caused by cryptorchidism.
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spelling pubmed-89323902022-04-11 miR-22-5p regulates the self-renewal of spermatogonial stem cells by targeting EZH2 Lv, Wenqiang Yu, Mei Su, Yilin Open Med (Wars) Research Article MiRNAs play an important role in spermatogonial stem cells (SSCs). The purpose of this study was to investigate the basic function of miR-22-5p in cryptorchidism. The results of RT-PCR, western blot, and immunohistochemistry showed that miR-22-5p was increased while EZH2 decreased in the testicular tissues of patients with cryptorchidism. Overexpression of miR-22-5p inhibited the proliferation of SSCs, increased cell apoptosis rate, and reduced expression of SSC marker proteins (GDNF and DAZL); however, knockout of miR-22-5p has the opposite effect. The Luciferase reporter gene assays demonstrated that EZH2 is a direct target of miR-22-5p. Moreover, EZH2 overexpression could reverse the effect of miR-22-5p mimic on SSCs’ proliferation, apoptosis, and expression of SSC marker proteins. Our results demonstrated that miR-22-5p regulates SSCs’ self-renewal by targeting EZH2, which indicated that miR-22-5p may serve as a biological marker for the treatment of infertility caused by cryptorchidism. De Gruyter 2022-03-17 /pmc/articles/PMC8932390/ /pubmed/35415251 http://dx.doi.org/10.1515/med-2022-0429 Text en © 2022 Wenqiang Lv et al., published by De Gruyter https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License.
spellingShingle Research Article
Lv, Wenqiang
Yu, Mei
Su, Yilin
miR-22-5p regulates the self-renewal of spermatogonial stem cells by targeting EZH2
title miR-22-5p regulates the self-renewal of spermatogonial stem cells by targeting EZH2
title_full miR-22-5p regulates the self-renewal of spermatogonial stem cells by targeting EZH2
title_fullStr miR-22-5p regulates the self-renewal of spermatogonial stem cells by targeting EZH2
title_full_unstemmed miR-22-5p regulates the self-renewal of spermatogonial stem cells by targeting EZH2
title_short miR-22-5p regulates the self-renewal of spermatogonial stem cells by targeting EZH2
title_sort mir-22-5p regulates the self-renewal of spermatogonial stem cells by targeting ezh2
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8932390/
https://www.ncbi.nlm.nih.gov/pubmed/35415251
http://dx.doi.org/10.1515/med-2022-0429
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