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miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells
BACKGROUND: Although Helicobacter pylori infection is necessary for development of gastric adenocarcinoma (GAC), the underlying mechanism remains poorly defined. This study aimed to explore how miR-221 and miR-222 are dysregulated after H. pylori infection and how these 2 miRNAs are involved in path...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4576921/ https://www.ncbi.nlm.nih.gov/pubmed/26364844 http://dx.doi.org/10.12659/MSM.894324 |
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author | Liu, Wenneng Song, Nian Yao, Huihua Zhao, Liying Liu, Hao Li, Guoxin |
author_facet | Liu, Wenneng Song, Nian Yao, Huihua Zhao, Liying Liu, Hao Li, Guoxin |
author_sort | Liu, Wenneng |
collection | PubMed |
description | BACKGROUND: Although Helicobacter pylori infection is necessary for development of gastric adenocarcinoma (GAC), the underlying mechanism remains poorly defined. This study aimed to explore how miR-221 and miR-222 are dysregulated after H. pylori infection and how these 2 miRNAs are involved in pathological development of gastric cancer. MATERIAL/METHODS: qRT-PCR analysis was performed to quantify miR-221 and miR-222 expression in patients with H. pylori – induced chronic gastritis, H. pylori-negative healthy controls, and in gastric cancer tissues and the corresponding adjacent normal tissues. Cell models were used to verify the expression profile. Dual luciferase assay was performed to verify putative binding between miR-221 or miR-222 and RECK. A loss-and-gain function study was performed to assess the miR-221/miR-222-RECK axis in gastric cancer cells. RESULTS: H. pylori infection leads to significantly higher miR-221 and miR-222 expression. MiR-221 and miR-222 can bind the same sequence of RECK 3′UTR, thereby modulating its expression. Through simultaneous regulation over RECK, miR-221 and miR-222 can promote gastric cancer cell growth and invasion. CONCLUSIONS: The miR-221/miR-222-RECK axis might be an important path modulating H. pylori infection-related gastric cancer development. |
format | Online Article Text |
id | pubmed-4576921 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-45769212015-09-30 miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells Liu, Wenneng Song, Nian Yao, Huihua Zhao, Liying Liu, Hao Li, Guoxin Med Sci Monit Molecular Biology BACKGROUND: Although Helicobacter pylori infection is necessary for development of gastric adenocarcinoma (GAC), the underlying mechanism remains poorly defined. This study aimed to explore how miR-221 and miR-222 are dysregulated after H. pylori infection and how these 2 miRNAs are involved in pathological development of gastric cancer. MATERIAL/METHODS: qRT-PCR analysis was performed to quantify miR-221 and miR-222 expression in patients with H. pylori – induced chronic gastritis, H. pylori-negative healthy controls, and in gastric cancer tissues and the corresponding adjacent normal tissues. Cell models were used to verify the expression profile. Dual luciferase assay was performed to verify putative binding between miR-221 or miR-222 and RECK. A loss-and-gain function study was performed to assess the miR-221/miR-222-RECK axis in gastric cancer cells. RESULTS: H. pylori infection leads to significantly higher miR-221 and miR-222 expression. MiR-221 and miR-222 can bind the same sequence of RECK 3′UTR, thereby modulating its expression. Through simultaneous regulation over RECK, miR-221 and miR-222 can promote gastric cancer cell growth and invasion. CONCLUSIONS: The miR-221/miR-222-RECK axis might be an important path modulating H. pylori infection-related gastric cancer development. International Scientific Literature, Inc. 2015-09-13 /pmc/articles/PMC4576921/ /pubmed/26364844 http://dx.doi.org/10.12659/MSM.894324 Text en © Med Sci Monit, 2015 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License |
spellingShingle | Molecular Biology Liu, Wenneng Song, Nian Yao, Huihua Zhao, Liying Liu, Hao Li, Guoxin miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells |
title | miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells |
title_full | miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells |
title_fullStr | miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells |
title_full_unstemmed | miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells |
title_short | miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells |
title_sort | mir-221 and mir-222 simultaneously target reck and regulate growth and invasion of gastric cancer cells |
topic | Molecular Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4576921/ https://www.ncbi.nlm.nih.gov/pubmed/26364844 http://dx.doi.org/10.12659/MSM.894324 |
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