Document Detail


Differential effects of TGF-beta1 on telomerase activity in thyroid carcinoma cell lines.
MedLine Citation:
PMID:  16288728     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The aim of the present study was to investigate the effect of transforming growth factor-beta1 (TGF-beta1) on telomerase activity in a panel of human anaplastic thyroid carcinoma (ATC) cell lines. Addition of TGF-beta1 decreased the telomerase activity in HTh 74 and KTC-1 cells, while in C 643 and HTh 7 an increased activity was observed. The decreased telomerase activity appeared to be due to transcriptional repression of the hTERT promoter. Addition of a PI-3 kinase inhibitor (LY294002) abrogated the stimulatory effect of TGF-beta1 on the telomerase activity, indicating the possible involvement of hTERT activation via phosphorylation. Furthermore, the MEK-inhibitor U0126 had similar effects suggesting dual regulatory mechanisms. Interestingly, the cell lines differed genetically in that ATC cell lines responding with increased telomerase activity harbored a p53 mutation. In conclusion, TGF-beta1 exerts opposing effects on telomerase activity in ATC cell lines, possibly reflecting deregulation of TGF-beta1 signaling in a more malignant genotype.
Authors:
Anna Lindkvist; Asa Franzén; Zhi-Ping Ren; Nils-Erik Heldin; Ylva Paulsson-Karlsson
Related Documents :
14607648 - Can inhibition of telomerase increase pancreatic cancer cell's susceptibility to chemot...
15974878 - Extratelomeric functions of telomerase.
20167708 - Targeting telomerase: t-cell friendly fire.
6630508 - Influence of anatomic site and age on the replication and differentiation of rat adipoc...
18651278 - A new cell-based fe model for the mechanics of embryonic epithelia.
12924928 - Thresholds of nitric oxide-mediated toxicity in human lymphoblastoid cells.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-11-02
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  338     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2005 Dec 
Date Detail:
Created Date:  2005-11-18     Completed Date:  2006-01-06     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1625-33     Citation Subset:  IM    
Affiliation:
Department of Genetics and Pathology, Uppsala University Hospital, Rudbeck Laboratory, SE-751 85 Uppsala, Sweden.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / antagonists & inhibitors,  metabolism
Cell Line, Tumor
Down-Regulation / drug effects
Genotype
Humans
Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors,  metabolism
Mutation / genetics
Promoter Regions, Genetic / genetics
Protein Kinase Inhibitors / pharmacology
Proto-Oncogene Proteins c-myc / genetics
RNA, Messenger / genetics,  metabolism
Telomerase / genetics,  metabolism*
Thyroid Neoplasms / enzymology*,  genetics,  metabolism
Transcription, Genetic / drug effects,  genetics
Transforming Growth Factor beta / pharmacology*
Transforming Growth Factor beta1
Tumor Suppressor Protein p53 / genetics
Chemical
Reg. No./Substance:
0/MYC protein, human; 0/Protein Kinase Inhibitors; 0/Proto-Oncogene Proteins c-myc; 0/RNA, Messenger; 0/TGFB1 protein, human; 0/Transforming Growth Factor beta; 0/Transforming Growth Factor beta1; 0/Tumor Suppressor Protein p53; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases; EC 2.7.7.49/Telomerase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Cell-mediated LDL oxidation: the impact of transition metals and transferrin.
Next Document:  Effects of peripheral inflammation on activation of ERK in the rostral ventromedial medulla.