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MiR-205 mediated APC regulation contributes to pancreatic cancer cell proliferation
BACKGROUND: Pancreatic cancer is a deadly malignancy with aggressive properties. MicroRNAs (miRNAs) participate in the pathogenesis of a variety of diseases and molecular processes by targeting functional mRNAs. Nevertheless, the regulatory role of miRNAs in signaling pathways involved in pancreatic...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676546/ https://www.ncbi.nlm.nih.gov/pubmed/31391772 http://dx.doi.org/10.3748/wjg.v25.i28.3775 |
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author | Qin, Rui-Feng Zhang, Jia Huo, Hao-Ran Yuan, Zeng-Jiang Xue, Jia-Dong |
author_facet | Qin, Rui-Feng Zhang, Jia Huo, Hao-Ran Yuan, Zeng-Jiang Xue, Jia-Dong |
author_sort | Qin, Rui-Feng |
collection | PubMed |
description | BACKGROUND: Pancreatic cancer is a deadly malignancy with aggressive properties. MicroRNAs (miRNAs) participate in the pathogenesis of a variety of diseases and molecular processes by targeting functional mRNAs. Nevertheless, the regulatory role of miRNAs in signaling pathways involved in pancreatic cancer remains largely unknown. AIM: To explore the molecular regulation involved in pancreatic cancer and potential mechanisms of miR-205. METHODS: Microarray analysis was performed to investigate the expression profile of miRNAs in pancreatic cancer. Expression of miR-205 was validated by qRT-PCR. Target prediction and functional enrichment analysis were employed to seek potential target genes of miR-205 and potential functions of these genes. The target binding of miR-205 and adenomatous polyposis coli (APC) was validated by luciferase reporter assay. APC protein expression in pancreatic cancer was validated by qRT-PCR and Western blot. Proliferation was evaluated by MTT and colony formation assays. RESULTS: A large number of miRNAs with altered expression were identified in pancreatic cancer. MiR-205 was significantly up-regulated. APC was found to be a validated target of miR-205 and down-regulated in pancreatic cancer. Proliferation experiments showed that miR-205 could promote cell proliferation in pancreatic cancer by targeting APC. CONCLUSION: The above findings suggested that miR-205 mediated APC regulation contributes to pancreatic cancer development, which could be considered as a novel prognostic biomarker for clinical care. |
format | Online Article Text |
id | pubmed-6676546 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-66765462019-08-07 MiR-205 mediated APC regulation contributes to pancreatic cancer cell proliferation Qin, Rui-Feng Zhang, Jia Huo, Hao-Ran Yuan, Zeng-Jiang Xue, Jia-Dong World J Gastroenterol Basic Study BACKGROUND: Pancreatic cancer is a deadly malignancy with aggressive properties. MicroRNAs (miRNAs) participate in the pathogenesis of a variety of diseases and molecular processes by targeting functional mRNAs. Nevertheless, the regulatory role of miRNAs in signaling pathways involved in pancreatic cancer remains largely unknown. AIM: To explore the molecular regulation involved in pancreatic cancer and potential mechanisms of miR-205. METHODS: Microarray analysis was performed to investigate the expression profile of miRNAs in pancreatic cancer. Expression of miR-205 was validated by qRT-PCR. Target prediction and functional enrichment analysis were employed to seek potential target genes of miR-205 and potential functions of these genes. The target binding of miR-205 and adenomatous polyposis coli (APC) was validated by luciferase reporter assay. APC protein expression in pancreatic cancer was validated by qRT-PCR and Western blot. Proliferation was evaluated by MTT and colony formation assays. RESULTS: A large number of miRNAs with altered expression were identified in pancreatic cancer. MiR-205 was significantly up-regulated. APC was found to be a validated target of miR-205 and down-regulated in pancreatic cancer. Proliferation experiments showed that miR-205 could promote cell proliferation in pancreatic cancer by targeting APC. CONCLUSION: The above findings suggested that miR-205 mediated APC regulation contributes to pancreatic cancer development, which could be considered as a novel prognostic biomarker for clinical care. Baishideng Publishing Group Inc 2019-07-28 2019-07-28 /pmc/articles/PMC6676546/ /pubmed/31391772 http://dx.doi.org/10.3748/wjg.v25.i28.3775 Text en ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. |
spellingShingle | Basic Study Qin, Rui-Feng Zhang, Jia Huo, Hao-Ran Yuan, Zeng-Jiang Xue, Jia-Dong MiR-205 mediated APC regulation contributes to pancreatic cancer cell proliferation |
title | MiR-205 mediated APC regulation contributes to pancreatic cancer cell proliferation |
title_full | MiR-205 mediated APC regulation contributes to pancreatic cancer cell proliferation |
title_fullStr | MiR-205 mediated APC regulation contributes to pancreatic cancer cell proliferation |
title_full_unstemmed | MiR-205 mediated APC regulation contributes to pancreatic cancer cell proliferation |
title_short | MiR-205 mediated APC regulation contributes to pancreatic cancer cell proliferation |
title_sort | mir-205 mediated apc regulation contributes to pancreatic cancer cell proliferation |
topic | Basic Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676546/ https://www.ncbi.nlm.nih.gov/pubmed/31391772 http://dx.doi.org/10.3748/wjg.v25.i28.3775 |
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