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LINC01355 suppresses breast cancer growth through FOXO3-mediated transcriptional repression of CCND1

Previously, several protein-coding tumor suppressors localized at 1p36 have been reported. In the present work, we focus on functional long non-coding RNAs (lncRNAs) embedded in this locus. Small interfering RNA was used to identify lncRNA candidates with growth-suppressive activities in breast canc...

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Autores principales: Ai, Bolun, Kong, Xiangyi, Wang, Xiangyu, Zhang, Kai, Yang, Xue, Zhai, Jie, Gao, Ran, Qi, Yihang, Wang, Jing, Wang, Zhongzhao, Fang, Yi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6594972/
https://www.ncbi.nlm.nih.gov/pubmed/31243265
http://dx.doi.org/10.1038/s41419-019-1741-8
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author Ai, Bolun
Kong, Xiangyi
Wang, Xiangyu
Zhang, Kai
Yang, Xue
Zhai, Jie
Gao, Ran
Qi, Yihang
Wang, Jing
Wang, Zhongzhao
Fang, Yi
author_facet Ai, Bolun
Kong, Xiangyi
Wang, Xiangyu
Zhang, Kai
Yang, Xue
Zhai, Jie
Gao, Ran
Qi, Yihang
Wang, Jing
Wang, Zhongzhao
Fang, Yi
author_sort Ai, Bolun
collection PubMed
description Previously, several protein-coding tumor suppressors localized at 1p36 have been reported. In the present work, we focus on functional long non-coding RNAs (lncRNAs) embedded in this locus. Small interfering RNA was used to identify lncRNA candidates with growth-suppressive activities in breast cancer. The mechanism involved was also explored. LINC01355 were downregulated in breast cancer cells relative to non-malignant breast epithelial cells. Overexpression of LINC01355 significantly inhibited proliferation, colony formation, and tumorigenesis of breast cancer cells. LINC01355 arrested breast cancer cells at the G0/G1 phase by repressing CCND1. Moreover, LINC01355 interacted with and stabilized FOXO3 protein, leading to transcriptional repression of CCND1. Importantly, LINC01355-mediated suppression of breast cancer growth was reversed by knockdown of FOXO3 or overexpression of CCND1. Clinically, LINC01355 was downregulated in breast cancer specimens and correlated with more aggressive features. There was a negative correlation between LINC01355 and CCND1 expression in breast cancer samples. LINC01355 acts as a tumor suppressor in breast cancer, which is ascribed to enhancement of FOXO3-mediated transcriptional repression of CCND1. Re-expression of LINC01355 may provide a potential therapeutic strategy to block breast cancer growth and progression.
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spelling pubmed-65949722019-06-27 LINC01355 suppresses breast cancer growth through FOXO3-mediated transcriptional repression of CCND1 Ai, Bolun Kong, Xiangyi Wang, Xiangyu Zhang, Kai Yang, Xue Zhai, Jie Gao, Ran Qi, Yihang Wang, Jing Wang, Zhongzhao Fang, Yi Cell Death Dis Article Previously, several protein-coding tumor suppressors localized at 1p36 have been reported. In the present work, we focus on functional long non-coding RNAs (lncRNAs) embedded in this locus. Small interfering RNA was used to identify lncRNA candidates with growth-suppressive activities in breast cancer. The mechanism involved was also explored. LINC01355 were downregulated in breast cancer cells relative to non-malignant breast epithelial cells. Overexpression of LINC01355 significantly inhibited proliferation, colony formation, and tumorigenesis of breast cancer cells. LINC01355 arrested breast cancer cells at the G0/G1 phase by repressing CCND1. Moreover, LINC01355 interacted with and stabilized FOXO3 protein, leading to transcriptional repression of CCND1. Importantly, LINC01355-mediated suppression of breast cancer growth was reversed by knockdown of FOXO3 or overexpression of CCND1. Clinically, LINC01355 was downregulated in breast cancer specimens and correlated with more aggressive features. There was a negative correlation between LINC01355 and CCND1 expression in breast cancer samples. LINC01355 acts as a tumor suppressor in breast cancer, which is ascribed to enhancement of FOXO3-mediated transcriptional repression of CCND1. Re-expression of LINC01355 may provide a potential therapeutic strategy to block breast cancer growth and progression. Nature Publishing Group UK 2019-06-26 /pmc/articles/PMC6594972/ /pubmed/31243265 http://dx.doi.org/10.1038/s41419-019-1741-8 Text en © The Author(s) 2019 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
Ai, Bolun
Kong, Xiangyi
Wang, Xiangyu
Zhang, Kai
Yang, Xue
Zhai, Jie
Gao, Ran
Qi, Yihang
Wang, Jing
Wang, Zhongzhao
Fang, Yi
LINC01355 suppresses breast cancer growth through FOXO3-mediated transcriptional repression of CCND1
title LINC01355 suppresses breast cancer growth through FOXO3-mediated transcriptional repression of CCND1
title_full LINC01355 suppresses breast cancer growth through FOXO3-mediated transcriptional repression of CCND1
title_fullStr LINC01355 suppresses breast cancer growth through FOXO3-mediated transcriptional repression of CCND1
title_full_unstemmed LINC01355 suppresses breast cancer growth through FOXO3-mediated transcriptional repression of CCND1
title_short LINC01355 suppresses breast cancer growth through FOXO3-mediated transcriptional repression of CCND1
title_sort linc01355 suppresses breast cancer growth through foxo3-mediated transcriptional repression of ccnd1
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6594972/
https://www.ncbi.nlm.nih.gov/pubmed/31243265
http://dx.doi.org/10.1038/s41419-019-1741-8
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