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Silencing of the hTERT gene through RNA interference induces apoptosis via Bax/Bcl-2 in human glioma cells

Glioma cells are characterized by their invasiveness and resistance to conventional therapeutics. The downregulation of human telomerase reverse transcriptase (hTERT) can lead to decreased cell proliferation and/or the induction of apoptotic cell death in cancer cells but has rarely been reported in...

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Autores principales: WANG, TUO, XUE, YAN, WANG, MAODE, SUN, QIANG
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3583528/
https://www.ncbi.nlm.nih.gov/pubmed/22895663
http://dx.doi.org/10.3892/or.2012.1952
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author WANG, TUO
XUE, YAN
WANG, MAODE
SUN, QIANG
author_facet WANG, TUO
XUE, YAN
WANG, MAODE
SUN, QIANG
author_sort WANG, TUO
collection PubMed
description Glioma cells are characterized by their invasiveness and resistance to conventional therapeutics. The downregulation of human telomerase reverse transcriptase (hTERT) can lead to decreased cell proliferation and/or the induction of apoptotic cell death in cancer cells but has rarely been reported in glioma cells. Here, we assessed the effect of the silencing of the hTERT gene on cell apoptosis and its possible molecular mechanism in T98G glioma cells. We found that the silencing of the hTERT gene in T98G cells significantly decreased cell proliferation and telomerase activity, increased the number of cells in G1 phase and decreased the number of cells in S phase, and induced apoptosis via decreasing the protein level of Bcl-2 and c-Myc and increasing the protein levels of Bax and p53.
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spelling pubmed-35835282013-02-28 Silencing of the hTERT gene through RNA interference induces apoptosis via Bax/Bcl-2 in human glioma cells WANG, TUO XUE, YAN WANG, MAODE SUN, QIANG Oncol Rep Articles Glioma cells are characterized by their invasiveness and resistance to conventional therapeutics. The downregulation of human telomerase reverse transcriptase (hTERT) can lead to decreased cell proliferation and/or the induction of apoptotic cell death in cancer cells but has rarely been reported in glioma cells. Here, we assessed the effect of the silencing of the hTERT gene on cell apoptosis and its possible molecular mechanism in T98G glioma cells. We found that the silencing of the hTERT gene in T98G cells significantly decreased cell proliferation and telomerase activity, increased the number of cells in G1 phase and decreased the number of cells in S phase, and induced apoptosis via decreasing the protein level of Bcl-2 and c-Myc and increasing the protein levels of Bax and p53. D.A. Spandidos 2012-10 2012-08-06 /pmc/articles/PMC3583528/ /pubmed/22895663 http://dx.doi.org/10.3892/or.2012.1952 Text en Copyright © 2012, 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
WANG, TUO
XUE, YAN
WANG, MAODE
SUN, QIANG
Silencing of the hTERT gene through RNA interference induces apoptosis via Bax/Bcl-2 in human glioma cells
title Silencing of the hTERT gene through RNA interference induces apoptosis via Bax/Bcl-2 in human glioma cells
title_full Silencing of the hTERT gene through RNA interference induces apoptosis via Bax/Bcl-2 in human glioma cells
title_fullStr Silencing of the hTERT gene through RNA interference induces apoptosis via Bax/Bcl-2 in human glioma cells
title_full_unstemmed Silencing of the hTERT gene through RNA interference induces apoptosis via Bax/Bcl-2 in human glioma cells
title_short Silencing of the hTERT gene through RNA interference induces apoptosis via Bax/Bcl-2 in human glioma cells
title_sort silencing of the htert gene through rna interference induces apoptosis via bax/bcl-2 in human glioma cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3583528/
https://www.ncbi.nlm.nih.gov/pubmed/22895663
http://dx.doi.org/10.3892/or.2012.1952
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