miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9 in H. pylori gastric cancer models

Abstract Helicobacter pylori (H. pylori) is one of the most important factors that affect the development of gastric cancer, and its mechanism remains un-elucidated. Our present study found that, miR-30a is crucial for regulating the growth and migration of H. pylori infected gastric cancer in vitro...

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Autores principales:	Xuan Liu, Qing Ji, Chengcheng Zhang, Xiaowei Liu, Yanna Liu, Ningning Liu, Hua Sui, Lihong Zhou, Songpo Wang, Qi Li
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e06fa079dadf4636ab887ef7eb4d0cdc
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spelling	oai:doaj.org-article:e06fa079dadf4636ab887ef7eb4d0cdc2021-12-02T11:52:33ZmiR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9 in H. pylori gastric cancer models10.1038/s41598-017-07193-w2045-2322https://doaj.org/article/e06fa079dadf4636ab887ef7eb4d0cdc2017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07193-whttps://doaj.org/toc/2045-2322Abstract Helicobacter pylori (H. pylori) is one of the most important factors that affect the development of gastric cancer, and its mechanism remains un-elucidated. Our present study found that, miR-30a is crucial for regulating the growth and migration of H. pylori infected gastric cancer in vitro by targeting COX-2 and BCL9. In details, double-stranded miR-30a precursor produced two single-stranded and matured miRNAs including miR-30a-3p and miR-30a-5p, which played significant biological functions in two different manners. First, miR-30a-3p inhibited COX-2 expression and regulated nuclear translocation of β-catenin, and second, miR-30a-5p targeted BCL9 to regulate TCF/LEF promoter activity followed by affecting β-catenin downstream target gene expression. In vivo, miR-30a knockout mice were successfully achieved using CRISPR/Cas9 gene editing technology. Compared with H. pylori-infected wild-type mice, H. pylori-infected miR-30a knockout mice showed increased incidence of chronic gastritis, chronic atrophic gastritis, atypical hyperplasia, and other precancerous lesions or adenocarcinoma manifestations in the antral or gastric mucosa of mice, as well as regulation of genes closely associated with tumor development. Taken together, miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9, and significantly affects the development of H. pylori-induced gastric cancer, shedding new light on the mechanisms underlying H. pylori-associated gastric cancer.Xuan LiuQing JiChengcheng ZhangXiaowei LiuYanna LiuNingning LiuHua SuiLihong ZhouSongpo WangQi LiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-15 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xuan Liu Qing Ji Chengcheng Zhang Xiaowei Liu Yanna Liu Ningning Liu Hua Sui Lihong Zhou Songpo Wang Qi Li miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9 in H. pylori gastric cancer models
description	Abstract Helicobacter pylori (H. pylori) is one of the most important factors that affect the development of gastric cancer, and its mechanism remains un-elucidated. Our present study found that, miR-30a is crucial for regulating the growth and migration of H. pylori infected gastric cancer in vitro by targeting COX-2 and BCL9. In details, double-stranded miR-30a precursor produced two single-stranded and matured miRNAs including miR-30a-3p and miR-30a-5p, which played significant biological functions in two different manners. First, miR-30a-3p inhibited COX-2 expression and regulated nuclear translocation of β-catenin, and second, miR-30a-5p targeted BCL9 to regulate TCF/LEF promoter activity followed by affecting β-catenin downstream target gene expression. In vivo, miR-30a knockout mice were successfully achieved using CRISPR/Cas9 gene editing technology. Compared with H. pylori-infected wild-type mice, H. pylori-infected miR-30a knockout mice showed increased incidence of chronic gastritis, chronic atrophic gastritis, atypical hyperplasia, and other precancerous lesions or adenocarcinoma manifestations in the antral or gastric mucosa of mice, as well as regulation of genes closely associated with tumor development. Taken together, miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9, and significantly affects the development of H. pylori-induced gastric cancer, shedding new light on the mechanisms underlying H. pylori-associated gastric cancer.
format	article
author	Xuan Liu Qing Ji Chengcheng Zhang Xiaowei Liu Yanna Liu Ningning Liu Hua Sui Lihong Zhou Songpo Wang Qi Li
author_facet	Xuan Liu Qing Ji Chengcheng Zhang Xiaowei Liu Yanna Liu Ningning Liu Hua Sui Lihong Zhou Songpo Wang Qi Li
author_sort	Xuan Liu
title	miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9 in H. pylori gastric cancer models
title_short	miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9 in H. pylori gastric cancer models
title_full	miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9 in H. pylori gastric cancer models
title_fullStr	miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9 in H. pylori gastric cancer models
title_full_unstemmed	miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9 in H. pylori gastric cancer models
title_sort	mir-30a acts as a tumor suppressor by double-targeting cox-2 and bcl9 in h. pylori gastric cancer models
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/e06fa079dadf4636ab887ef7eb4d0cdc
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miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9 in H. pylori gastric cancer models

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