Table of Contents Author Guidelines Submit a Manuscript

An erratum for this article has been published. To view the erratum, please click here.

Journal of Thyroid Research
Volume 2011, Article ID 856050, 8 pages
Research Article

Cell-Type-Dependent Thyroid Hormone Effects on Glioma Tumor Cell Lines

1Department of Pharmacology, University of Athens, 75 Mikras Asias Avenue,11527 Goudi, Athens, Greece
2School of Pharmacy and Biomedical Sciences, University of Central Lancashire, Preston PR1 2HE, Lancashire, UK

Received 5 August 2011; Revised 24 September 2011; Accepted 24 September 2011

Academic Editor: Fausto Bogazzi

Copyright © 2011 Liappas Alexandros et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Purpose. The present study investigated the potential effects of long-term T3 treatment on glioma tumor cell lines. Thyroid hormone action on cell growth, differentiation and survival during development may be of therapeutic relevance Methods and Results 1321N1 cell line, an astrocytoma grade II, and U87MG, a glioblastoma grade IV, were exposed for 2 and 4 days in medium deprived of T3 and in medium containing 1 nM T3. T3 promoted re-differentiation in both cell lines. However, T3 increased cell proliferation in 1321N1 (2 days) which declined thereafter (4 days) while in U87MG resulted in suppression of cell proliferation. At the molecular level, a 2.9 fold increase in the expression of TRα1 receptor was observed in U87MG versus 1321N1, P < 0.05. TRβ1 receptor was undetectable. These changes corresponded to a distinct pattern of T3-induced kinase signaling activation; T3 had no effect on ERK activation in both cell lines but significantly increased phospho-Akt levels in 1321N1. Conclusion. In conclusion, T3 can re-differentiate glioma tumor cells, whereas its effect on cell proliferation appears to be dependent on the type of tumor cell line with aggressive tumors being more sensitive to T3. TRα1 receptor may, at least in part, be implicated in this response.