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Influence of far upstream element binding protein 1 gene on chemotherapy sensitivity in human U251 glioblastoma cells

INTRODUCTION: The aim of this study was to determine the influence of the far upstream element binding protein 1 gene (FUBP1) on chemotherapy sensitivity in human U251 glioblastoma cells. MATERIAL AND METHODS: Real-time polymerase chain reaction (PCR) was used to determine the expression of the FUBP...

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Autores principales: Hong, Yang, Shi, Yu, Shang, Chao, Xue, Yixue, Liu, Yunhui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4754377/
https://www.ncbi.nlm.nih.gov/pubmed/26925132
http://dx.doi.org/10.5114/aoms.2016.57592
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author Hong, Yang
Shi, Yu
Shang, Chao
Xue, Yixue
Liu, Yunhui
author_facet Hong, Yang
Shi, Yu
Shang, Chao
Xue, Yixue
Liu, Yunhui
author_sort Hong, Yang
collection PubMed
description INTRODUCTION: The aim of this study was to determine the influence of the far upstream element binding protein 1 gene (FUBP1) on chemotherapy sensitivity in human U251 glioblastoma cells. MATERIAL AND METHODS: Real-time polymerase chain reaction (PCR) was used to determine the expression of the FUBP1 gene in 43 cases of human brain gliomas. Western blot analysis was used to determine the inhibitory effect of RNA interference on FUBP1 gene expression. Methyl thiazolyl tetrazolium assay (MTT) and flow cytometry methods were used to determine the growth inhibitory rate and apoptosis rate of the U251 cells with FUBP1 silencing. The growth inhibitory rate and apoptosis rate were further determined after treatment of those U251 cells with cisplatin (DDP). RESULTS: The expression of FUBP1 mRNA was up-regulated significantly in gliomas, 177.65% as much as in peri-cancerous tissues (p < 0.05). The expression of FUBP1 protein was inhibited significantly with siRNA-FUBP1 (p < 0.05). In FUBP1-silenced cells, the growth inhibitory rate increased from 1.4% to 29.5%, and the apoptosis rate increased from 2.68% to 5.84% (p < 0.05 for both). After treating with DDP at various concentrations (1, 3, 5 µg/ml), the growth inhibitory rate of FUBP1-silenced cells increased from 14.42%, 17.46% and 23.55% to 21.69%, 27.51% and 37.57%; the apoptosis rate increased from 8.85%, 14.37% and 18.21% to 13.25%, 18.46% and 26.52%. CONCLUSIONS: The up-regulation of FUBP1 relates to the carcinogenesis of gliomas. FUBP1 silencing increases the growth inhibitory rate and apoptosis rate of the U251 cells, and enhances the chemotherapy sensitivity of U251 cells to DDP.
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spelling pubmed-47543772016-02-26 Influence of far upstream element binding protein 1 gene on chemotherapy sensitivity in human U251 glioblastoma cells Hong, Yang Shi, Yu Shang, Chao Xue, Yixue Liu, Yunhui Arch Med Sci Basic Research INTRODUCTION: The aim of this study was to determine the influence of the far upstream element binding protein 1 gene (FUBP1) on chemotherapy sensitivity in human U251 glioblastoma cells. MATERIAL AND METHODS: Real-time polymerase chain reaction (PCR) was used to determine the expression of the FUBP1 gene in 43 cases of human brain gliomas. Western blot analysis was used to determine the inhibitory effect of RNA interference on FUBP1 gene expression. Methyl thiazolyl tetrazolium assay (MTT) and flow cytometry methods were used to determine the growth inhibitory rate and apoptosis rate of the U251 cells with FUBP1 silencing. The growth inhibitory rate and apoptosis rate were further determined after treatment of those U251 cells with cisplatin (DDP). RESULTS: The expression of FUBP1 mRNA was up-regulated significantly in gliomas, 177.65% as much as in peri-cancerous tissues (p < 0.05). The expression of FUBP1 protein was inhibited significantly with siRNA-FUBP1 (p < 0.05). In FUBP1-silenced cells, the growth inhibitory rate increased from 1.4% to 29.5%, and the apoptosis rate increased from 2.68% to 5.84% (p < 0.05 for both). After treating with DDP at various concentrations (1, 3, 5 µg/ml), the growth inhibitory rate of FUBP1-silenced cells increased from 14.42%, 17.46% and 23.55% to 21.69%, 27.51% and 37.57%; the apoptosis rate increased from 8.85%, 14.37% and 18.21% to 13.25%, 18.46% and 26.52%. CONCLUSIONS: The up-regulation of FUBP1 relates to the carcinogenesis of gliomas. FUBP1 silencing increases the growth inhibitory rate and apoptosis rate of the U251 cells, and enhances the chemotherapy sensitivity of U251 cells to DDP. Termedia Publishing House 2016-02-02 2016-02-01 /pmc/articles/PMC4754377/ /pubmed/26925132 http://dx.doi.org/10.5114/aoms.2016.57592 Text en Copyright © 2016 Termedia & Banach http://creativecommons.org/licenses/by-nc-sa/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
spellingShingle Basic Research
Hong, Yang
Shi, Yu
Shang, Chao
Xue, Yixue
Liu, Yunhui
Influence of far upstream element binding protein 1 gene on chemotherapy sensitivity in human U251 glioblastoma cells
title Influence of far upstream element binding protein 1 gene on chemotherapy sensitivity in human U251 glioblastoma cells
title_full Influence of far upstream element binding protein 1 gene on chemotherapy sensitivity in human U251 glioblastoma cells
title_fullStr Influence of far upstream element binding protein 1 gene on chemotherapy sensitivity in human U251 glioblastoma cells
title_full_unstemmed Influence of far upstream element binding protein 1 gene on chemotherapy sensitivity in human U251 glioblastoma cells
title_short Influence of far upstream element binding protein 1 gene on chemotherapy sensitivity in human U251 glioblastoma cells
title_sort influence of far upstream element binding protein 1 gene on chemotherapy sensitivity in human u251 glioblastoma cells
topic Basic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4754377/
https://www.ncbi.nlm.nih.gov/pubmed/26925132
http://dx.doi.org/10.5114/aoms.2016.57592
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