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Long non‐coding RNA MYOSLID functions as a competing endogenous RNA to regulate MCL‐1 expression by sponging miR‐29c‐3p in gastric cancer

OBJECTIVE: Long non‐coding RNA (lncRNA) has become an important regulator of many human malignancies. However, the biological role and clinical significance of most lncRNA in gastric cancer (GC) remain unclear. METHODS: We investigate the biological function, mechanism of action and clinical express...

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Autores principales: Han, Yuying, Wu, Nan, Jiang, Mingzuo, Chu, Yi, Wang, Zhiyang, Liu, Hao, Cao, Jiayi, Liu, Hanming, Xu, Bing, Xie, Xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6869334/
https://www.ncbi.nlm.nih.gov/pubmed/31497917
http://dx.doi.org/10.1111/cpr.12678
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author Han, Yuying
Wu, Nan
Jiang, Mingzuo
Chu, Yi
Wang, Zhiyang
Liu, Hao
Cao, Jiayi
Liu, Hanming
Xu, Bing
Xie, Xin
author_facet Han, Yuying
Wu, Nan
Jiang, Mingzuo
Chu, Yi
Wang, Zhiyang
Liu, Hao
Cao, Jiayi
Liu, Hanming
Xu, Bing
Xie, Xin
author_sort Han, Yuying
collection PubMed
description OBJECTIVE: Long non‐coding RNA (lncRNA) has become an important regulator of many human malignancies. However, the biological role and clinical significance of most lncRNA in gastric cancer (GC) remain unclear. METHODS: We investigate the biological function, mechanism of action and clinical expression of lncRNA MYOSLID in GC. First, we analysed the differential expression of lncRNA MYOSLID in GC tissues and non‐cancerous tissues by analysing the sequencing data obtained from The Cancer Genome Atlas. Subsequently, we verified that lncRNA MYOSLID regulates the proliferation and apoptosis of GC cells by acting as a ceRNA against miR‐29c‐3p. The nude mouse xenograft was used to further confirm the functional significance of lncRNA MYOSLID in vivo. RESULTS: We found for the first time that the expression of lncRNA MYOSLID was significantly up‐regulated in GC tissues, and the up‐regulation of lncRNA MYOSLID in GC was correlated with tumour size, AJCC stage, depth of invasion and survival time. In addition, apoptosis and growth arrest can be induced in vitro after knockdown of lncRNA MYOSLID, which inhibits tumorigenesis in mouse xenografts in vivo. Further in‐depth studies revealed that lncRNA MYOSLID acts as a ceRNA of miR‐29c‐3p, resulting in de‐repression of its downstream target gene MCL‐1. CONCLUSION: The lncRNA MYOSLID‐miR‐29c‐3p‐MCL‐1 axis plays a key role in the development of GC. Our findings may provide potential new targets for the diagnosis and treatment of human GC.
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spelling pubmed-68693342020-03-13 Long non‐coding RNA MYOSLID functions as a competing endogenous RNA to regulate MCL‐1 expression by sponging miR‐29c‐3p in gastric cancer Han, Yuying Wu, Nan Jiang, Mingzuo Chu, Yi Wang, Zhiyang Liu, Hao Cao, Jiayi Liu, Hanming Xu, Bing Xie, Xin Cell Prolif Original Articles OBJECTIVE: Long non‐coding RNA (lncRNA) has become an important regulator of many human malignancies. However, the biological role and clinical significance of most lncRNA in gastric cancer (GC) remain unclear. METHODS: We investigate the biological function, mechanism of action and clinical expression of lncRNA MYOSLID in GC. First, we analysed the differential expression of lncRNA MYOSLID in GC tissues and non‐cancerous tissues by analysing the sequencing data obtained from The Cancer Genome Atlas. Subsequently, we verified that lncRNA MYOSLID regulates the proliferation and apoptosis of GC cells by acting as a ceRNA against miR‐29c‐3p. The nude mouse xenograft was used to further confirm the functional significance of lncRNA MYOSLID in vivo. RESULTS: We found for the first time that the expression of lncRNA MYOSLID was significantly up‐regulated in GC tissues, and the up‐regulation of lncRNA MYOSLID in GC was correlated with tumour size, AJCC stage, depth of invasion and survival time. In addition, apoptosis and growth arrest can be induced in vitro after knockdown of lncRNA MYOSLID, which inhibits tumorigenesis in mouse xenografts in vivo. Further in‐depth studies revealed that lncRNA MYOSLID acts as a ceRNA of miR‐29c‐3p, resulting in de‐repression of its downstream target gene MCL‐1. CONCLUSION: The lncRNA MYOSLID‐miR‐29c‐3p‐MCL‐1 axis plays a key role in the development of GC. Our findings may provide potential new targets for the diagnosis and treatment of human GC. John Wiley and Sons Inc. 2019-09-09 /pmc/articles/PMC6869334/ /pubmed/31497917 http://dx.doi.org/10.1111/cpr.12678 Text en © 2019 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Han, Yuying
Wu, Nan
Jiang, Mingzuo
Chu, Yi
Wang, Zhiyang
Liu, Hao
Cao, Jiayi
Liu, Hanming
Xu, Bing
Xie, Xin
Long non‐coding RNA MYOSLID functions as a competing endogenous RNA to regulate MCL‐1 expression by sponging miR‐29c‐3p in gastric cancer
title Long non‐coding RNA MYOSLID functions as a competing endogenous RNA to regulate MCL‐1 expression by sponging miR‐29c‐3p in gastric cancer
title_full Long non‐coding RNA MYOSLID functions as a competing endogenous RNA to regulate MCL‐1 expression by sponging miR‐29c‐3p in gastric cancer
title_fullStr Long non‐coding RNA MYOSLID functions as a competing endogenous RNA to regulate MCL‐1 expression by sponging miR‐29c‐3p in gastric cancer
title_full_unstemmed Long non‐coding RNA MYOSLID functions as a competing endogenous RNA to regulate MCL‐1 expression by sponging miR‐29c‐3p in gastric cancer
title_short Long non‐coding RNA MYOSLID functions as a competing endogenous RNA to regulate MCL‐1 expression by sponging miR‐29c‐3p in gastric cancer
title_sort long non‐coding rna myoslid functions as a competing endogenous rna to regulate mcl‐1 expression by sponging mir‐29c‐3p in gastric cancer
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6869334/
https://www.ncbi.nlm.nih.gov/pubmed/31497917
http://dx.doi.org/10.1111/cpr.12678
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