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RNAi-mediated knockdown of E2F2 inhibits tumorigenicity of human glioblastoma cells
In a previous genome-wide expression profiling study, we identified E2F2 as a hyperexpressed gene in stem-like cells of distinct glioblastoma multiforme (GBM) specimens. Since the encoded E2F2 transcription factor has been implicated in both tumor suppression and tumor development, we conducted a fu...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4156183/ https://www.ncbi.nlm.nih.gov/pubmed/25202354 http://dx.doi.org/10.3892/ol.2014.2369 |
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author | NAKAHATA, ADRIANA M. SUZUKI, DANIELA E. RODINI, CAROLINA O. FIUZA, MAYARA L. OKAMOTO, OSWALDO K. |
author_facet | NAKAHATA, ADRIANA M. SUZUKI, DANIELA E. RODINI, CAROLINA O. FIUZA, MAYARA L. OKAMOTO, OSWALDO K. |
author_sort | NAKAHATA, ADRIANA M. |
collection | PubMed |
description | In a previous genome-wide expression profiling study, we identified E2F2 as a hyperexpressed gene in stem-like cells of distinct glioblastoma multiforme (GBM) specimens. Since the encoded E2F2 transcription factor has been implicated in both tumor suppression and tumor development, we conducted a functional study to investigate the pertinence of E2F2 to human gliomagenesis. E2F2 expression was knocked down by transfecting U87MG cells with plasmids carrying a specific silencing shRNA. Upon E2F2 silencing, in vitro cell proliferation was significantly reduced, as indicated by a time-course analysis of viable tumor cells. Anchorage-independent cell growth was also significantly inhibited after E2F2 silencing, based on cell colony formation in soft agar. Subcutaneous and orthotopic xenograft models of GBM in nude mice also indicated inhibition of tumor development in vivo, following E2F2 silencing. As expression of the E2F2 gene is associated with glioblastoma stem cells and is involved in the transformation of human astrocytes, the present findings suggest that E2F2 is involved in gliomagenesis and could be explored as a potential therapeutic target in malignant gliomas. |
format | Online Article Text |
id | pubmed-4156183 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-41561832014-09-08 RNAi-mediated knockdown of E2F2 inhibits tumorigenicity of human glioblastoma cells NAKAHATA, ADRIANA M. SUZUKI, DANIELA E. RODINI, CAROLINA O. FIUZA, MAYARA L. OKAMOTO, OSWALDO K. Oncol Lett Articles In a previous genome-wide expression profiling study, we identified E2F2 as a hyperexpressed gene in stem-like cells of distinct glioblastoma multiforme (GBM) specimens. Since the encoded E2F2 transcription factor has been implicated in both tumor suppression and tumor development, we conducted a functional study to investigate the pertinence of E2F2 to human gliomagenesis. E2F2 expression was knocked down by transfecting U87MG cells with plasmids carrying a specific silencing shRNA. Upon E2F2 silencing, in vitro cell proliferation was significantly reduced, as indicated by a time-course analysis of viable tumor cells. Anchorage-independent cell growth was also significantly inhibited after E2F2 silencing, based on cell colony formation in soft agar. Subcutaneous and orthotopic xenograft models of GBM in nude mice also indicated inhibition of tumor development in vivo, following E2F2 silencing. As expression of the E2F2 gene is associated with glioblastoma stem cells and is involved in the transformation of human astrocytes, the present findings suggest that E2F2 is involved in gliomagenesis and could be explored as a potential therapeutic target in malignant gliomas. D.A. Spandidos 2014-10 2014-07-22 /pmc/articles/PMC4156183/ /pubmed/25202354 http://dx.doi.org/10.3892/ol.2014.2369 Text en Copyright © 2014, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Articles NAKAHATA, ADRIANA M. SUZUKI, DANIELA E. RODINI, CAROLINA O. FIUZA, MAYARA L. OKAMOTO, OSWALDO K. RNAi-mediated knockdown of E2F2 inhibits tumorigenicity of human glioblastoma cells |
title | RNAi-mediated knockdown of E2F2 inhibits tumorigenicity of human glioblastoma cells |
title_full | RNAi-mediated knockdown of E2F2 inhibits tumorigenicity of human glioblastoma cells |
title_fullStr | RNAi-mediated knockdown of E2F2 inhibits tumorigenicity of human glioblastoma cells |
title_full_unstemmed | RNAi-mediated knockdown of E2F2 inhibits tumorigenicity of human glioblastoma cells |
title_short | RNAi-mediated knockdown of E2F2 inhibits tumorigenicity of human glioblastoma cells |
title_sort | rnai-mediated knockdown of e2f2 inhibits tumorigenicity of human glioblastoma cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4156183/ https://www.ncbi.nlm.nih.gov/pubmed/25202354 http://dx.doi.org/10.3892/ol.2014.2369 |
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