Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/38258
Title: RNAi-mediated knockdown of E2F2 inhibits tumorigenicity of human glioblastoma cells
Authors: Nakahata, Adriana Miti [UNIFESP]
Suzuki, Daniela Emi [UNIFESP]
Rodini, Carolina de Oliveira [UNIFESP]
Fiuza, Mayara L.
Okamoto, Oswaldo K.
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Keywords: E2F2
glioblastoma multiforme
cancer
tumorigenesis
Issue Date: 1-Oct-2014
Publisher: Spandidos Publ Ltd
Citation: Oncology Letters. Athens: Spandidos Publ Ltd, v. 8, n. 4, p. 1487-1491, 2014.
Abstract: 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.
URI: http://repositorio.unifesp.br/handle/11600/38258
ISSN: 1792-1074
Other Identifiers: http://dx.doi.org/10.3892/ol.2014.2369
Appears in Collections:Em verificação - Geral

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.