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FGFR1 is an independent prognostic factor and can be regulated by miR-497 in gastric cancer progression

Fibroblast growth factor receptor 1 (FGFR1) has been reported in gastric cancer to be a prognostic factor. However, miR-497-targeted FGFR1 has not been explored in the carcinogenesis of gastric cancer. The present study intended to revalidate the prognostic significance of FGFR1 in patients with gas...

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Autores principales: Xie, Gang, Ke, Qi, Ji, Yu Zu, Wang, An-qun, Jing, Meng, Zou, li-li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Associação Brasileira de Divulgação Científica 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6262748/
https://www.ncbi.nlm.nih.gov/pubmed/30484492
http://dx.doi.org/10.1590/1414-431X20187816
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author Xie, Gang
Ke, Qi
Ji, Yu Zu
Wang, An-qun
Jing, Meng
Zou, li-li
author_facet Xie, Gang
Ke, Qi
Ji, Yu Zu
Wang, An-qun
Jing, Meng
Zou, li-li
author_sort Xie, Gang
collection PubMed
description Fibroblast growth factor receptor 1 (FGFR1) has been reported in gastric cancer to be a prognostic factor. However, miR-497-targeted FGFR1 has not been explored in the carcinogenesis of gastric cancer. The present study intended to revalidate the prognostic significance of FGFR1 in patients with gastric cancer, and the mechanism of miR-497-regulated FGFR1 was investigated in gastric cancer cell proliferation and apoptosis. The messenger RNA (mRNA) and protein levels were assayed by RT-qPCR and western blotting, respectively. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. Cell proliferation was analyzed by CCK-8 assay. Annexin V-FITC/PI staining was used to evaluate the apoptosis in AGS and SGC-7901 cells. FGFR1 was frequently up-regulated in gastric cancer tissues and associated with poor overall survival in patients with gastric cancer. Interestingly, FGFR1 loss-of-function resulted in a significant growth inhibition and apoptosis in AGS and SGC-7901 cells. In addition, we found that miR-497 was inhibited in gastric cancer tissues and cell lines, while overexpression of miR-497 could suppress proliferation and induce apoptosis in AGS and SGC-7901 cells. Importantly, bioinformatics analysis and experimental data suggested that FGFR1 was a direct target of miR-497, which could inhibit FGFR1 expression when transfected with miR-497 mimics. Furthermore, we found that overexpression of FGFR1 reversed the growth inhibition and apoptosis of miR-497 mimics in AGS and SGC-7901 cells. These findings suggested that overexpression of miR-497 inhibited proliferation and induced apoptosis in gastric cancer through the suppression of FGFR1.
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spelling pubmed-62627482018-12-19 FGFR1 is an independent prognostic factor and can be regulated by miR-497 in gastric cancer progression Xie, Gang Ke, Qi Ji, Yu Zu Wang, An-qun Jing, Meng Zou, li-li Braz J Med Biol Res Research Article Fibroblast growth factor receptor 1 (FGFR1) has been reported in gastric cancer to be a prognostic factor. However, miR-497-targeted FGFR1 has not been explored in the carcinogenesis of gastric cancer. The present study intended to revalidate the prognostic significance of FGFR1 in patients with gastric cancer, and the mechanism of miR-497-regulated FGFR1 was investigated in gastric cancer cell proliferation and apoptosis. The messenger RNA (mRNA) and protein levels were assayed by RT-qPCR and western blotting, respectively. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. Cell proliferation was analyzed by CCK-8 assay. Annexin V-FITC/PI staining was used to evaluate the apoptosis in AGS and SGC-7901 cells. FGFR1 was frequently up-regulated in gastric cancer tissues and associated with poor overall survival in patients with gastric cancer. Interestingly, FGFR1 loss-of-function resulted in a significant growth inhibition and apoptosis in AGS and SGC-7901 cells. In addition, we found that miR-497 was inhibited in gastric cancer tissues and cell lines, while overexpression of miR-497 could suppress proliferation and induce apoptosis in AGS and SGC-7901 cells. Importantly, bioinformatics analysis and experimental data suggested that FGFR1 was a direct target of miR-497, which could inhibit FGFR1 expression when transfected with miR-497 mimics. Furthermore, we found that overexpression of FGFR1 reversed the growth inhibition and apoptosis of miR-497 mimics in AGS and SGC-7901 cells. These findings suggested that overexpression of miR-497 inhibited proliferation and induced apoptosis in gastric cancer through the suppression of FGFR1. Associação Brasileira de Divulgação Científica 2018-11-23 /pmc/articles/PMC6262748/ /pubmed/30484492 http://dx.doi.org/10.1590/1414-431X20187816 Text en https://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Xie, Gang
Ke, Qi
Ji, Yu Zu
Wang, An-qun
Jing, Meng
Zou, li-li
FGFR1 is an independent prognostic factor and can be regulated by miR-497 in gastric cancer progression
title FGFR1 is an independent prognostic factor and can be regulated by miR-497 in gastric cancer progression
title_full FGFR1 is an independent prognostic factor and can be regulated by miR-497 in gastric cancer progression
title_fullStr FGFR1 is an independent prognostic factor and can be regulated by miR-497 in gastric cancer progression
title_full_unstemmed FGFR1 is an independent prognostic factor and can be regulated by miR-497 in gastric cancer progression
title_short FGFR1 is an independent prognostic factor and can be regulated by miR-497 in gastric cancer progression
title_sort fgfr1 is an independent prognostic factor and can be regulated by mir-497 in gastric cancer progression
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6262748/
https://www.ncbi.nlm.nih.gov/pubmed/30484492
http://dx.doi.org/10.1590/1414-431X20187816
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