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LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge

Long non-coding RNAs (lncRNAs), which are important functional regulators in cancer, have received increased attention in recent years. In this study, next-generation sequencing technology was used to identify aberrantly expressed lncRNAs in follicular thyroid carcinoma (FTC). The long non-coding RN...

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Autores principales: Liang, Leilei, Xu, Jingchao, Wang, Meng, Xu, Gaoran, Zhang, Ning, Wang, Guangzhi, Zhao, Yongfu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5841368/
https://www.ncbi.nlm.nih.gov/pubmed/29515098
http://dx.doi.org/10.1038/s41419-018-0382-7
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author Liang, Leilei
Xu, Jingchao
Wang, Meng
Xu, Gaoran
Zhang, Ning
Wang, Guangzhi
Zhao, Yongfu
author_facet Liang, Leilei
Xu, Jingchao
Wang, Meng
Xu, Gaoran
Zhang, Ning
Wang, Guangzhi
Zhao, Yongfu
author_sort Liang, Leilei
collection PubMed
description Long non-coding RNAs (lncRNAs), which are important functional regulators in cancer, have received increased attention in recent years. In this study, next-generation sequencing technology was used to identify aberrantly expressed lncRNAs in follicular thyroid carcinoma (FTC). The long non-coding RNA–HLA complex P5 (HCP5) was found to be overexpressed in FTC. The results of the qPCR analysis were consistent with the sequencing results. In addition, functional experiments showed that overexpression of HCP5 can promote the proliferation, migration, invasiveness and angiogenic ability of FTC cells. Furthermore, according to the sequencing results, HCP5 and alpha-2, 6-sialyltransferase 2 (ST6GAL2) were co-expressed in FTC. We hypothesised that ST6GAL2 may be regulated by HCP5, which would in turn mediate the activity of FTC cells. Through qPCR, immunostaining analyses and functional experiments, we determined that the expression of HCP5 was elevated and was correlated with the levels of ST6GAL2 in FTC tissues and cells. Mechanistic experiments showed that HCP5 functions as a competing endogenous RNA (ceRNA) and acts as a sponge for miR-22-3p, miR-186-5p and miR-216a-5p, which activates ST6GAL2. In summary, our study revealed that HCP5 is a tumour regulator in the development of FTC and that it may contribute to improvement of FTC diagnosis and therapy.
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spelling pubmed-58413682018-03-09 LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge Liang, Leilei Xu, Jingchao Wang, Meng Xu, Gaoran Zhang, Ning Wang, Guangzhi Zhao, Yongfu Cell Death Dis Article Long non-coding RNAs (lncRNAs), which are important functional regulators in cancer, have received increased attention in recent years. In this study, next-generation sequencing technology was used to identify aberrantly expressed lncRNAs in follicular thyroid carcinoma (FTC). The long non-coding RNA–HLA complex P5 (HCP5) was found to be overexpressed in FTC. The results of the qPCR analysis were consistent with the sequencing results. In addition, functional experiments showed that overexpression of HCP5 can promote the proliferation, migration, invasiveness and angiogenic ability of FTC cells. Furthermore, according to the sequencing results, HCP5 and alpha-2, 6-sialyltransferase 2 (ST6GAL2) were co-expressed in FTC. We hypothesised that ST6GAL2 may be regulated by HCP5, which would in turn mediate the activity of FTC cells. Through qPCR, immunostaining analyses and functional experiments, we determined that the expression of HCP5 was elevated and was correlated with the levels of ST6GAL2 in FTC tissues and cells. Mechanistic experiments showed that HCP5 functions as a competing endogenous RNA (ceRNA) and acts as a sponge for miR-22-3p, miR-186-5p and miR-216a-5p, which activates ST6GAL2. In summary, our study revealed that HCP5 is a tumour regulator in the development of FTC and that it may contribute to improvement of FTC diagnosis and therapy. Nature Publishing Group UK 2018-03-07 /pmc/articles/PMC5841368/ /pubmed/29515098 http://dx.doi.org/10.1038/s41419-018-0382-7 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Liang, Leilei
Xu, Jingchao
Wang, Meng
Xu, Gaoran
Zhang, Ning
Wang, Guangzhi
Zhao, Yongfu
LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge
title LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge
title_full LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge
title_fullStr LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge
title_full_unstemmed LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge
title_short LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge
title_sort lncrna hcp5 promotes follicular thyroid carcinoma progression via mirnas sponge
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5841368/
https://www.ncbi.nlm.nih.gov/pubmed/29515098
http://dx.doi.org/10.1038/s41419-018-0382-7
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