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AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO
The androgen receptor (AR) and its related signaling pathways play an important role in the development of prostate cancer (PCa). Long non-coding RNAs (lncRNAs) are involved in the regulation of tumorigenesis and development, but their specific mechanism of action remains unclear. This study examine...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8625561/ https://www.ncbi.nlm.nih.gov/pubmed/34833084 http://dx.doi.org/10.3390/life11111208 |
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author | Lu, Yali Wan, Xuechao Huang, Wenhua Zhang, Lu Luo, Jun Li, Dujian Huang, Yan Li, Yao Xu, Yaoting |
author_facet | Lu, Yali Wan, Xuechao Huang, Wenhua Zhang, Lu Luo, Jun Li, Dujian Huang, Yan Li, Yao Xu, Yaoting |
author_sort | Lu, Yali |
collection | PubMed |
description | The androgen receptor (AR) and its related signaling pathways play an important role in the development of prostate cancer (PCa). Long non-coding RNAs (lncRNAs) are involved in the regulation of tumorigenesis and development, but their specific mechanism of action remains unclear. This study examines the function and mechanisms of action of lncRNA AC016745.3 in the development of PCa. It shows that dihydrotestosterone (DHT) results in the AR-dependent suppression of AC016745.3 expression in the LNCaP androgen-sensitive human prostate adenocarcinoma cell line. In addition, overexpression of AC016745.3 inhibits the proliferation and migration of PCa cells, and suppresses the expression of AR target genes. This research also demonstrates that the protein NONO interacts with AR and functions as an AR co-activator, promoting AR transcriptional activity. Furthermore, using RNA immunoprecipitation (RIP)-PCR experiments, the study demonstrates that both NONO and AR can bind AC016745.3. Moreover, cell phenotypic experiments reveal that NONO can promote cellular proliferation and migration, and that AC016745.3 can partially antagonize the pro-oncogenic functions of NONO in PCa cells. In summary, the results indicate that AC016745.3 can bind NONO, suppressing its ability to promote AR-dependent transcriptional activity. Furthermore, DHT-dependent suppression of AC016745.3 expression can enhance NONO’s promotion effect on AR. |
format | Online Article Text |
id | pubmed-8625561 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-86255612021-11-27 AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO Lu, Yali Wan, Xuechao Huang, Wenhua Zhang, Lu Luo, Jun Li, Dujian Huang, Yan Li, Yao Xu, Yaoting Life (Basel) Article The androgen receptor (AR) and its related signaling pathways play an important role in the development of prostate cancer (PCa). Long non-coding RNAs (lncRNAs) are involved in the regulation of tumorigenesis and development, but their specific mechanism of action remains unclear. This study examines the function and mechanisms of action of lncRNA AC016745.3 in the development of PCa. It shows that dihydrotestosterone (DHT) results in the AR-dependent suppression of AC016745.3 expression in the LNCaP androgen-sensitive human prostate adenocarcinoma cell line. In addition, overexpression of AC016745.3 inhibits the proliferation and migration of PCa cells, and suppresses the expression of AR target genes. This research also demonstrates that the protein NONO interacts with AR and functions as an AR co-activator, promoting AR transcriptional activity. Furthermore, using RNA immunoprecipitation (RIP)-PCR experiments, the study demonstrates that both NONO and AR can bind AC016745.3. Moreover, cell phenotypic experiments reveal that NONO can promote cellular proliferation and migration, and that AC016745.3 can partially antagonize the pro-oncogenic functions of NONO in PCa cells. In summary, the results indicate that AC016745.3 can bind NONO, suppressing its ability to promote AR-dependent transcriptional activity. Furthermore, DHT-dependent suppression of AC016745.3 expression can enhance NONO’s promotion effect on AR. MDPI 2021-11-09 /pmc/articles/PMC8625561/ /pubmed/34833084 http://dx.doi.org/10.3390/life11111208 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Lu, Yali Wan, Xuechao Huang, Wenhua Zhang, Lu Luo, Jun Li, Dujian Huang, Yan Li, Yao Xu, Yaoting AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title | AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title_full | AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title_fullStr | AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title_full_unstemmed | AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title_short | AC016745.3 Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title_sort | ac016745.3 regulates the transcription of ar target genes by antagonizing nono |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8625561/ https://www.ncbi.nlm.nih.gov/pubmed/34833084 http://dx.doi.org/10.3390/life11111208 |
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