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The Long Non-Coding RNA IDH1-AS1 Promotes Prostate Cancer Progression by Enhancing IDH1 Enzyme Activity

PURPOSE: Long non-coding RNAs (lncRNAs) are involved in the development of various tumors including prostate cancer. The purpose of this study was to explore the function of a natural antisense RNA, IDH1-AS1, exerting potential carcinogenic effects in prostate cancer through a novel molecular mechan...

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Autores principales: Wu, Shuo, Ding, Liucheng, Xu, Hewei, Gao, Jie, Shao, Yunpeng, Zhang, Sicong, Wei, Zhongqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432214/
https://www.ncbi.nlm.nih.gov/pubmed/32884284
http://dx.doi.org/10.2147/OTT.S251915
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author Wu, Shuo
Ding, Liucheng
Xu, Hewei
Gao, Jie
Shao, Yunpeng
Zhang, Sicong
Wei, Zhongqing
author_facet Wu, Shuo
Ding, Liucheng
Xu, Hewei
Gao, Jie
Shao, Yunpeng
Zhang, Sicong
Wei, Zhongqing
author_sort Wu, Shuo
collection PubMed
description PURPOSE: Long non-coding RNAs (lncRNAs) are involved in the development of various tumors including prostate cancer. The purpose of this study was to explore the function of a natural antisense RNA, IDH1-AS1, exerting potential carcinogenic effects in prostate cancer through a novel molecular mechanism. MATERIALS AND METHODS: GEPIA and CCLE databases were searched to identify alterations in the expression of IDH1-AS1, which were then verified by RT-qPCR in 20 pairs of matched tumor and normal tissue samples. Subsequently, CCK-8, EdU, and transwell assays were conducted to investigate the carcinogenic effect of IDH1-AS1. RT-qPCR, Western blot, and isocitrate dehydrogenase 1 (IDH1) enzyme activity assays were used to explore the functional relationship between IDH1-AS1 and its sense gene IDH1. RESULTS: IDH1-AS1 expression was found to be significantly increased in prostate cancer tissues and cell lines. IDH1-AS1 knockdown significantly inhibited the proliferation and migration of prostate cancer cells. Interestingly, RT-qPCR and Western blot analyses revealed that IDH1-AS1 did not significantly affect the expression of IDH1 mRNA or protein but was involved in the regulation of IDH1 enzyme activity in prostate cancer cells. CONCLUSION: Our experiments revealed that the carcinogenic effects of IDH1-AS1 in prostate cancer may depend on a new molecular mechanism, which directly alters IDH1 enzyme activity. Our findings indicate that IDH1-AS1 is a novel candidate target for prostate cancer treatment.
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spelling pubmed-74322142020-09-02 The Long Non-Coding RNA IDH1-AS1 Promotes Prostate Cancer Progression by Enhancing IDH1 Enzyme Activity Wu, Shuo Ding, Liucheng Xu, Hewei Gao, Jie Shao, Yunpeng Zhang, Sicong Wei, Zhongqing Onco Targets Ther Original Research PURPOSE: Long non-coding RNAs (lncRNAs) are involved in the development of various tumors including prostate cancer. The purpose of this study was to explore the function of a natural antisense RNA, IDH1-AS1, exerting potential carcinogenic effects in prostate cancer through a novel molecular mechanism. MATERIALS AND METHODS: GEPIA and CCLE databases were searched to identify alterations in the expression of IDH1-AS1, which were then verified by RT-qPCR in 20 pairs of matched tumor and normal tissue samples. Subsequently, CCK-8, EdU, and transwell assays were conducted to investigate the carcinogenic effect of IDH1-AS1. RT-qPCR, Western blot, and isocitrate dehydrogenase 1 (IDH1) enzyme activity assays were used to explore the functional relationship between IDH1-AS1 and its sense gene IDH1. RESULTS: IDH1-AS1 expression was found to be significantly increased in prostate cancer tissues and cell lines. IDH1-AS1 knockdown significantly inhibited the proliferation and migration of prostate cancer cells. Interestingly, RT-qPCR and Western blot analyses revealed that IDH1-AS1 did not significantly affect the expression of IDH1 mRNA or protein but was involved in the regulation of IDH1 enzyme activity in prostate cancer cells. CONCLUSION: Our experiments revealed that the carcinogenic effects of IDH1-AS1 in prostate cancer may depend on a new molecular mechanism, which directly alters IDH1 enzyme activity. Our findings indicate that IDH1-AS1 is a novel candidate target for prostate cancer treatment. Dove 2020-08-07 /pmc/articles/PMC7432214/ /pubmed/32884284 http://dx.doi.org/10.2147/OTT.S251915 Text en © 2020 Wu et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Wu, Shuo
Ding, Liucheng
Xu, Hewei
Gao, Jie
Shao, Yunpeng
Zhang, Sicong
Wei, Zhongqing
The Long Non-Coding RNA IDH1-AS1 Promotes Prostate Cancer Progression by Enhancing IDH1 Enzyme Activity
title The Long Non-Coding RNA IDH1-AS1 Promotes Prostate Cancer Progression by Enhancing IDH1 Enzyme Activity
title_full The Long Non-Coding RNA IDH1-AS1 Promotes Prostate Cancer Progression by Enhancing IDH1 Enzyme Activity
title_fullStr The Long Non-Coding RNA IDH1-AS1 Promotes Prostate Cancer Progression by Enhancing IDH1 Enzyme Activity
title_full_unstemmed The Long Non-Coding RNA IDH1-AS1 Promotes Prostate Cancer Progression by Enhancing IDH1 Enzyme Activity
title_short The Long Non-Coding RNA IDH1-AS1 Promotes Prostate Cancer Progression by Enhancing IDH1 Enzyme Activity
title_sort long non-coding rna idh1-as1 promotes prostate cancer progression by enhancing idh1 enzyme activity
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432214/
https://www.ncbi.nlm.nih.gov/pubmed/32884284
http://dx.doi.org/10.2147/OTT.S251915
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