<i>AC016745.3</i> 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...
Guardado en:
Autores principales: | , , , , , , , , |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
MDPI AG
2021
|
Materias: | |
Acceso en línea: | https://doaj.org/article/7b223a770eb44a31a300146ebe6735d5 |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
id |
oai:doaj.org-article:7b223a770eb44a31a300146ebe6735d5 |
---|---|
record_format |
dspace |
spelling |
oai:doaj.org-article:7b223a770eb44a31a300146ebe6735d52021-11-25T18:11:12Z<i>AC016745.3</i> Regulates the Transcription of AR Target Genes by Antagonizing NONO10.3390/life111112082075-1729https://doaj.org/article/7b223a770eb44a31a300146ebe6735d52021-11-01T00:00:00Zhttps://www.mdpi.com/2075-1729/11/11/1208https://doaj.org/toc/2075-1729The 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 <i>AC016745.3</i> in the development of PCa. It shows that dihydrotestosterone (DHT) results in the AR-dependent suppression of <i>AC016745.3</i> expression in the LNCaP androgen-sensitive human prostate adenocarcinoma cell line. In addition, overexpression of <i>AC016745.3</i> 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 <i>AC016745.3</i>. Moreover, cell phenotypic experiments reveal that NONO can promote cellular proliferation and migration, and that <i>AC016745.3</i> can partially antagonize the pro-oncogenic functions of NONO in PCa cells. In summary, the results indicate that <i>AC016745.3</i> can bind NONO, suppressing its ability to promote AR-dependent transcriptional activity. Furthermore, DHT-dependent suppression of <i>AC016745.3</i> expression can enhance NONO’s promotion effect on AR.Yali LuXuechao WanWenhua HuangLu ZhangJun LuoDujian LiYan HuangYao LiYaoting XuMDPI AGarticleprostate cancerandrogen receptor<i>AC016745.3</i>NONOtranscriptional regulationScienceQENLife, Vol 11, Iss 1208, p 1208 (2021) |
institution |
DOAJ |
collection |
DOAJ |
language |
EN |
topic |
prostate cancer androgen receptor <i>AC016745.3</i> NONO transcriptional regulation Science Q |
spellingShingle |
prostate cancer androgen receptor <i>AC016745.3</i> NONO transcriptional regulation Science Q Yali Lu Xuechao Wan Wenhua Huang Lu Zhang Jun Luo Dujian Li Yan Huang Yao Li Yaoting Xu <i>AC016745.3</i> Regulates the Transcription of AR Target Genes by Antagonizing NONO |
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 <i>AC016745.3</i> in the development of PCa. It shows that dihydrotestosterone (DHT) results in the AR-dependent suppression of <i>AC016745.3</i> expression in the LNCaP androgen-sensitive human prostate adenocarcinoma cell line. In addition, overexpression of <i>AC016745.3</i> 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 <i>AC016745.3</i>. Moreover, cell phenotypic experiments reveal that NONO can promote cellular proliferation and migration, and that <i>AC016745.3</i> can partially antagonize the pro-oncogenic functions of NONO in PCa cells. In summary, the results indicate that <i>AC016745.3</i> can bind NONO, suppressing its ability to promote AR-dependent transcriptional activity. Furthermore, DHT-dependent suppression of <i>AC016745.3</i> expression can enhance NONO’s promotion effect on AR. |
format |
article |
author |
Yali Lu Xuechao Wan Wenhua Huang Lu Zhang Jun Luo Dujian Li Yan Huang Yao Li Yaoting Xu |
author_facet |
Yali Lu Xuechao Wan Wenhua Huang Lu Zhang Jun Luo Dujian Li Yan Huang Yao Li Yaoting Xu |
author_sort |
Yali Lu |
title |
<i>AC016745.3</i> Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title_short |
<i>AC016745.3</i> Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title_full |
<i>AC016745.3</i> Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title_fullStr |
<i>AC016745.3</i> Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title_full_unstemmed |
<i>AC016745.3</i> Regulates the Transcription of AR Target Genes by Antagonizing NONO |
title_sort |
<i>ac016745.3</i> regulates the transcription of ar target genes by antagonizing nono |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/7b223a770eb44a31a300146ebe6735d5 |
work_keys_str_mv |
AT yalilu iac0167453iregulatesthetranscriptionofartargetgenesbyantagonizingnono AT xuechaowan iac0167453iregulatesthetranscriptionofartargetgenesbyantagonizingnono AT wenhuahuang iac0167453iregulatesthetranscriptionofartargetgenesbyantagonizingnono AT luzhang iac0167453iregulatesthetranscriptionofartargetgenesbyantagonizingnono AT junluo iac0167453iregulatesthetranscriptionofartargetgenesbyantagonizingnono AT dujianli iac0167453iregulatesthetranscriptionofartargetgenesbyantagonizingnono AT yanhuang iac0167453iregulatesthetranscriptionofartargetgenesbyantagonizingnono AT yaoli iac0167453iregulatesthetranscriptionofartargetgenesbyantagonizingnono AT yaotingxu iac0167453iregulatesthetranscriptionofartargetgenesbyantagonizingnono |
_version_ |
1718411504843227136 |