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lncRNA UCA1 Functions as a ceRNA to Promote Prostate Cancer Progression via Sponging miR143

UCA1 (urothelial carcinoma associated 1) is a long non-coding RNA (lncRNA) that was found overexpressed in various human cancers including prostate cancer (PCa). However, the aspect of UCA1-miRNA-mRNA interaction in PCa remains unclear. In this study, we confirmed the role of UCA1 in PCa and found t...

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Detalles Bibliográficos
Autores principales: Yu, Yanlan, Gao, Fengbin, He, Qian, Li, Gonghui, Ding, Guoqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society of Gene & Cell Therapy 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6962633/
https://www.ncbi.nlm.nih.gov/pubmed/31954329
http://dx.doi.org/10.1016/j.omtn.2019.11.021
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author Yu, Yanlan
Gao, Fengbin
He, Qian
Li, Gonghui
Ding, Guoqing
author_facet Yu, Yanlan
Gao, Fengbin
He, Qian
Li, Gonghui
Ding, Guoqing
author_sort Yu, Yanlan
collection PubMed
description UCA1 (urothelial carcinoma associated 1) is a long non-coding RNA (lncRNA) that was found overexpressed in various human cancers including prostate cancer (PCa). However, the aspect of UCA1-miRNA-mRNA interaction in PCa remains unclear. In this study, we confirmed the role of UCA1 in PCa and found that UCA1 downregulation inhibited cell proliferation of PCa cells. Then we demonstrated that repressed UCA1 promoted the microRNA-143 (miR-143) expression and miR-143 could bind to the predicted binding site of UCA1. We then proved the anti-tumor role of miR-143 in PCa. Furthermore, we found that miR-143 displays its role in PCa via modulating the MYO6 expression. In summary, our study demonstrated that UCA1 exerts oncogenes activity in PCa, acting mechanistically by upregulating MYO6 expression through “sponging” miR-143.
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spelling pubmed-69626332020-01-22 lncRNA UCA1 Functions as a ceRNA to Promote Prostate Cancer Progression via Sponging miR143 Yu, Yanlan Gao, Fengbin He, Qian Li, Gonghui Ding, Guoqing Mol Ther Nucleic Acids Article UCA1 (urothelial carcinoma associated 1) is a long non-coding RNA (lncRNA) that was found overexpressed in various human cancers including prostate cancer (PCa). However, the aspect of UCA1-miRNA-mRNA interaction in PCa remains unclear. In this study, we confirmed the role of UCA1 in PCa and found that UCA1 downregulation inhibited cell proliferation of PCa cells. Then we demonstrated that repressed UCA1 promoted the microRNA-143 (miR-143) expression and miR-143 could bind to the predicted binding site of UCA1. We then proved the anti-tumor role of miR-143 in PCa. Furthermore, we found that miR-143 displays its role in PCa via modulating the MYO6 expression. In summary, our study demonstrated that UCA1 exerts oncogenes activity in PCa, acting mechanistically by upregulating MYO6 expression through “sponging” miR-143. American Society of Gene & Cell Therapy 2019-11-27 /pmc/articles/PMC6962633/ /pubmed/31954329 http://dx.doi.org/10.1016/j.omtn.2019.11.021 Text en © 2019 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Yu, Yanlan
Gao, Fengbin
He, Qian
Li, Gonghui
Ding, Guoqing
lncRNA UCA1 Functions as a ceRNA to Promote Prostate Cancer Progression via Sponging miR143
title lncRNA UCA1 Functions as a ceRNA to Promote Prostate Cancer Progression via Sponging miR143
title_full lncRNA UCA1 Functions as a ceRNA to Promote Prostate Cancer Progression via Sponging miR143
title_fullStr lncRNA UCA1 Functions as a ceRNA to Promote Prostate Cancer Progression via Sponging miR143
title_full_unstemmed lncRNA UCA1 Functions as a ceRNA to Promote Prostate Cancer Progression via Sponging miR143
title_short lncRNA UCA1 Functions as a ceRNA to Promote Prostate Cancer Progression via Sponging miR143
title_sort lncrna uca1 functions as a cerna to promote prostate cancer progression via sponging mir143
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6962633/
https://www.ncbi.nlm.nih.gov/pubmed/31954329
http://dx.doi.org/10.1016/j.omtn.2019.11.021
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