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Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCND1 expression

BACKGROUND: Recently, numerous studies have demonstrated the emerging role of long non-coding RNAs (lncRNAs) in human cancers. Linc00467 is a newly defined lncRNA and was reported to promote cell survival in neuroblastoma. However, the function of linc00467 in lung cancer is still unclear. MATERIAL...

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Autores principales: Ding, Hao, Luo, Yuchuan, Hu, Ke, Liu, Pei, Xiong, Mengqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6709798/
https://www.ncbi.nlm.nih.gov/pubmed/31686834
http://dx.doi.org/10.2147/OTT.S207748
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author Ding, Hao
Luo, Yuchuan
Hu, Ke
Liu, Pei
Xiong, Mengqing
author_facet Ding, Hao
Luo, Yuchuan
Hu, Ke
Liu, Pei
Xiong, Mengqing
author_sort Ding, Hao
collection PubMed
description BACKGROUND: Recently, numerous studies have demonstrated the emerging role of long non-coding RNAs (lncRNAs) in human cancers. Linc00467 is a newly defined lncRNA and was reported to promote cell survival in neuroblastoma. However, the function of linc00467 in lung cancer is still unclear. MATERIAL AND METHODS: We analyzed linc00467 expression and survival data derived from The Cancer Genome Altas lung adenocarcinoma (LUAD) dataset as well as in collected LUAD tissues. Then, we silenced linc00467 expression in two lung cancer cell lines using small interfering RNAs and explored the effect of linc00467 knockdown on cell growth in vitro and in vivo. Moreover, we revealed a novel target gene of linc00467 and elucidated the underlying competitive endogenous RNA regulatory mechanism in lung cancer cells. RESULTS: Our data suggested that linc00467 expression was elevated in LUAD tissues and correlated with overall survival of LUAD patients. Linc00467 knockdown resulted in reduced proliferation rate in lung cancer cells. Furthermore, we elucidated that linc00467 promoted CCND1 expression in lung cancer cells via functioning as a molecular sponge for miR-20b-5p. CONCLUSION: Linc00467/miR-20b-5p/CCND1 signaling pathway may provide new insights into lung cancer treatment.
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spelling pubmed-67097982019-11-04 Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCND1 expression Ding, Hao Luo, Yuchuan Hu, Ke Liu, Pei Xiong, Mengqing Onco Targets Ther Original Research BACKGROUND: Recently, numerous studies have demonstrated the emerging role of long non-coding RNAs (lncRNAs) in human cancers. Linc00467 is a newly defined lncRNA and was reported to promote cell survival in neuroblastoma. However, the function of linc00467 in lung cancer is still unclear. MATERIAL AND METHODS: We analyzed linc00467 expression and survival data derived from The Cancer Genome Altas lung adenocarcinoma (LUAD) dataset as well as in collected LUAD tissues. Then, we silenced linc00467 expression in two lung cancer cell lines using small interfering RNAs and explored the effect of linc00467 knockdown on cell growth in vitro and in vivo. Moreover, we revealed a novel target gene of linc00467 and elucidated the underlying competitive endogenous RNA regulatory mechanism in lung cancer cells. RESULTS: Our data suggested that linc00467 expression was elevated in LUAD tissues and correlated with overall survival of LUAD patients. Linc00467 knockdown resulted in reduced proliferation rate in lung cancer cells. Furthermore, we elucidated that linc00467 promoted CCND1 expression in lung cancer cells via functioning as a molecular sponge for miR-20b-5p. CONCLUSION: Linc00467/miR-20b-5p/CCND1 signaling pathway may provide new insights into lung cancer treatment. Dove 2019-08-21 /pmc/articles/PMC6709798/ /pubmed/31686834 http://dx.doi.org/10.2147/OTT.S207748 Text en © 2019 Ding 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
Ding, Hao
Luo, Yuchuan
Hu, Ke
Liu, Pei
Xiong, Mengqing
Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCND1 expression
title Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCND1 expression
title_full Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCND1 expression
title_fullStr Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCND1 expression
title_full_unstemmed Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCND1 expression
title_short Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCND1 expression
title_sort linc00467 promotes lung adenocarcinoma proliferation via sponging mir-20b-5p to activate ccnd1 expression
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6709798/
https://www.ncbi.nlm.nih.gov/pubmed/31686834
http://dx.doi.org/10.2147/OTT.S207748
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