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miR-511 and miR-1297 Inhibit Human Lung Adenocarcinoma Cell Proliferation by Targeting Oncogene TRIB2
microRNAs (miRNAs) are small noncoding RNAs that regulate genes and contribute to many kinds of human diseases, including cancer. Two miRNAs, miR-511 and miR-1297, were investigated for a possible role in adenocarcinoma based on predicted binding sites for the TRIB2 oncogene by microRNA analysis sof...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3465292/ https://www.ncbi.nlm.nih.gov/pubmed/23071539 http://dx.doi.org/10.1371/journal.pone.0046090 |
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author | Zhang, Chao Chi, Yong Liang Wang, Ping Yu Wang, Ya Qi Zhang, Yan Xia Deng, Jingti Lv, Chang Jun Xie, Shu Yang |
author_facet | Zhang, Chao Chi, Yong Liang Wang, Ping Yu Wang, Ya Qi Zhang, Yan Xia Deng, Jingti Lv, Chang Jun Xie, Shu Yang |
author_sort | Zhang, Chao |
collection | PubMed |
description | microRNAs (miRNAs) are small noncoding RNAs that regulate genes and contribute to many kinds of human diseases, including cancer. Two miRNAs, miR-511 and miR-1297, were investigated for a possible role in adenocarcinoma based on predicted binding sites for the TRIB2 oncogene by microRNA analysis software, and the pcDNA-GFP-TRIB2–3′UTR vector was constructed to investigate the interaction between TRIB2 and miR-511/1297 in the adenocarcinoma cell line A549. Green fluorescent protein (GFP) expression was estimated by fluorescence microscopy and flow cytometry after A549 cells were co-transfected with miR-511 (or miR-1297) and pcDNA-GFP-TRIB2–3′UTR vector. The expression of GFP in the miR-511- and miR-1297-treated cells was significantly downregulated in contrast with the negative-control (NC) miRNA-treated cells. The decreased expression of TRIB2 was further detected after miR-511 (or miR-1297) treatment by western blotting. The MTT test showed inhibition of A549 cell proliferation and Annexin V-FITC/PI dual staining showed increased apoptosis in the miR-511- and miR-1297-treated cells compared to the NC cultures. A transcription factor downstream of TRIB2, the CCAAT/enhancer-binding protein alpha (C/EBPα), was expression at higher levels after miR-511 (or miR-1297) decreasing TRIB2 expression. Our results illustrate that miR-511 and miR-1297 act as tumor suppressor genes, which could suppress A549 cell proliferation in vitro and in vivo by suppressing TRIB2 and further increasing C/EBPα expression. |
format | Online Article Text |
id | pubmed-3465292 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-34652922012-10-15 miR-511 and miR-1297 Inhibit Human Lung Adenocarcinoma Cell Proliferation by Targeting Oncogene TRIB2 Zhang, Chao Chi, Yong Liang Wang, Ping Yu Wang, Ya Qi Zhang, Yan Xia Deng, Jingti Lv, Chang Jun Xie, Shu Yang PLoS One Research Article microRNAs (miRNAs) are small noncoding RNAs that regulate genes and contribute to many kinds of human diseases, including cancer. Two miRNAs, miR-511 and miR-1297, were investigated for a possible role in adenocarcinoma based on predicted binding sites for the TRIB2 oncogene by microRNA analysis software, and the pcDNA-GFP-TRIB2–3′UTR vector was constructed to investigate the interaction between TRIB2 and miR-511/1297 in the adenocarcinoma cell line A549. Green fluorescent protein (GFP) expression was estimated by fluorescence microscopy and flow cytometry after A549 cells were co-transfected with miR-511 (or miR-1297) and pcDNA-GFP-TRIB2–3′UTR vector. The expression of GFP in the miR-511- and miR-1297-treated cells was significantly downregulated in contrast with the negative-control (NC) miRNA-treated cells. The decreased expression of TRIB2 was further detected after miR-511 (or miR-1297) treatment by western blotting. The MTT test showed inhibition of A549 cell proliferation and Annexin V-FITC/PI dual staining showed increased apoptosis in the miR-511- and miR-1297-treated cells compared to the NC cultures. A transcription factor downstream of TRIB2, the CCAAT/enhancer-binding protein alpha (C/EBPα), was expression at higher levels after miR-511 (or miR-1297) decreasing TRIB2 expression. Our results illustrate that miR-511 and miR-1297 act as tumor suppressor genes, which could suppress A549 cell proliferation in vitro and in vivo by suppressing TRIB2 and further increasing C/EBPα expression. Public Library of Science 2012-10-05 /pmc/articles/PMC3465292/ /pubmed/23071539 http://dx.doi.org/10.1371/journal.pone.0046090 Text en © 2012 Zhang et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Zhang, Chao Chi, Yong Liang Wang, Ping Yu Wang, Ya Qi Zhang, Yan Xia Deng, Jingti Lv, Chang Jun Xie, Shu Yang miR-511 and miR-1297 Inhibit Human Lung Adenocarcinoma Cell Proliferation by Targeting Oncogene TRIB2 |
title | miR-511 and miR-1297 Inhibit Human Lung Adenocarcinoma Cell Proliferation by Targeting Oncogene TRIB2
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title_full | miR-511 and miR-1297 Inhibit Human Lung Adenocarcinoma Cell Proliferation by Targeting Oncogene TRIB2
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title_fullStr | miR-511 and miR-1297 Inhibit Human Lung Adenocarcinoma Cell Proliferation by Targeting Oncogene TRIB2
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title_full_unstemmed | miR-511 and miR-1297 Inhibit Human Lung Adenocarcinoma Cell Proliferation by Targeting Oncogene TRIB2
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title_short | miR-511 and miR-1297 Inhibit Human Lung Adenocarcinoma Cell Proliferation by Targeting Oncogene TRIB2
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title_sort | mir-511 and mir-1297 inhibit human lung adenocarcinoma cell proliferation by targeting oncogene trib2 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3465292/ https://www.ncbi.nlm.nih.gov/pubmed/23071539 http://dx.doi.org/10.1371/journal.pone.0046090 |
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