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Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b

BACKGROUND: Long non-coding RNAs (lncRNAs) have emerged as important regulators of human cancers. However, the functional roles of lncRNAs and the mechanisms responsible for their aberrant expression in gastric cancer (GC) have not been well characterized. METHODS: In this study, we examined the exp...

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Autores principales: Zhang, Xu, Liang, Wei, Liu, Jibin, Zang, Xueyan, Gu, Jianmei, Pan, Lei, Shi, Hui, Fu, Min, Huang, Zhenhua, Zhang, Yu, Qian, Hui, Jiang, Pengcheng, Xu, Wenrong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6029056/
https://www.ncbi.nlm.nih.gov/pubmed/29970131
http://dx.doi.org/10.1186/s13046-018-0803-6
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author Zhang, Xu
Liang, Wei
Liu, Jibin
Zang, Xueyan
Gu, Jianmei
Pan, Lei
Shi, Hui
Fu, Min
Huang, Zhenhua
Zhang, Yu
Qian, Hui
Jiang, Pengcheng
Xu, Wenrong
author_facet Zhang, Xu
Liang, Wei
Liu, Jibin
Zang, Xueyan
Gu, Jianmei
Pan, Lei
Shi, Hui
Fu, Min
Huang, Zhenhua
Zhang, Yu
Qian, Hui
Jiang, Pengcheng
Xu, Wenrong
author_sort Zhang, Xu
collection PubMed
description BACKGROUND: Long non-coding RNAs (lncRNAs) have emerged as important regulators of human cancers. However, the functional roles of lncRNAs and the mechanisms responsible for their aberrant expression in gastric cancer (GC) have not been well characterized. METHODS: In this study, we examined the expression of lncRNA UFC1 in GC by qRT-PCR and explored its correlation with clinicopathological parameters. In vitro cell functional assays and in vivo animal studies were performed to determine the roles of UFC1 in GC progression. RESULTS: UFC1 was elevated and predicted poorer prognosis in GC. UFC1 knockdown inhibited while UFC1 overexpression promoted GC cell proliferation, migration, and invasion. UFC1 bound to miR-498 to antagonize its tumor suppressive effect on Lin28b. Suppression of Lin28b by miR-498 could be rescued by UFC1 overexpression, whereas Lin28b overexpression partially rescued UFC1 knockdown-mediated inhibition of GC cell function. Lin28b expression was increased in GC and suggested a co-expression pattern with UFC1. CONCLUSIONS: UFC1 has a promoting role in GC progression, at least in part, by acting as a miR-498 sponge and derepressing Lin28b expression, which would provide a novel biomarker for GC diagnosis and prognosis and offer a potential target for GC therapy. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13046-018-0803-6) contains supplementary material, which is available to authorized users.
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spelling pubmed-60290562018-07-09 Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b Zhang, Xu Liang, Wei Liu, Jibin Zang, Xueyan Gu, Jianmei Pan, Lei Shi, Hui Fu, Min Huang, Zhenhua Zhang, Yu Qian, Hui Jiang, Pengcheng Xu, Wenrong J Exp Clin Cancer Res Research BACKGROUND: Long non-coding RNAs (lncRNAs) have emerged as important regulators of human cancers. However, the functional roles of lncRNAs and the mechanisms responsible for their aberrant expression in gastric cancer (GC) have not been well characterized. METHODS: In this study, we examined the expression of lncRNA UFC1 in GC by qRT-PCR and explored its correlation with clinicopathological parameters. In vitro cell functional assays and in vivo animal studies were performed to determine the roles of UFC1 in GC progression. RESULTS: UFC1 was elevated and predicted poorer prognosis in GC. UFC1 knockdown inhibited while UFC1 overexpression promoted GC cell proliferation, migration, and invasion. UFC1 bound to miR-498 to antagonize its tumor suppressive effect on Lin28b. Suppression of Lin28b by miR-498 could be rescued by UFC1 overexpression, whereas Lin28b overexpression partially rescued UFC1 knockdown-mediated inhibition of GC cell function. Lin28b expression was increased in GC and suggested a co-expression pattern with UFC1. CONCLUSIONS: UFC1 has a promoting role in GC progression, at least in part, by acting as a miR-498 sponge and derepressing Lin28b expression, which would provide a novel biomarker for GC diagnosis and prognosis and offer a potential target for GC therapy. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13046-018-0803-6) contains supplementary material, which is available to authorized users. BioMed Central 2018-07-03 /pmc/articles/PMC6029056/ /pubmed/29970131 http://dx.doi.org/10.1186/s13046-018-0803-6 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Zhang, Xu
Liang, Wei
Liu, Jibin
Zang, Xueyan
Gu, Jianmei
Pan, Lei
Shi, Hui
Fu, Min
Huang, Zhenhua
Zhang, Yu
Qian, Hui
Jiang, Pengcheng
Xu, Wenrong
Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b
title Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b
title_full Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b
title_fullStr Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b
title_full_unstemmed Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b
title_short Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b
title_sort long non-coding rna ufc1 promotes gastric cancer progression by regulating mir-498/lin28b
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6029056/
https://www.ncbi.nlm.nih.gov/pubmed/29970131
http://dx.doi.org/10.1186/s13046-018-0803-6
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