Telomerase is regulated by c-Jun NH2-Terminal kinase in ovarian surface epithelial cells

Telomerase activity is present in >90% of all tumors and appears to be regulated by the phosphatidylinositol 3-kinase signaling pathway. Here we demonstrate that Akt is not involved in the signaling cascade for telomerase regulation in ovarian surface epithelial cells. However, we showed that c-J...

Full description

Saved in:
Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 2002-08, Vol.62 (16), p.4575-4578
Main Authors: ALFNNSN-DE MATTE, Mirhellp Y, HUA YANG, EVANS, Myria S, CHENG, Jin O, KRUK, Patricia A
Format: Article
Language:English
Subjects:
Anisomycin - pharmacology
Biological and medical sciences
Cell physiology
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
DNA-Binding Proteins
Enzyme Induction - drug effects
Epithelial Cells - enzymology
Female
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Enzymologic
Gene Expression Regulation, Neoplastic
Humans
JNK Mitogen-Activated Protein Kinases
Mitogen-Activated Protein Kinases - genetics
Mitogen-Activated Protein Kinases - metabolism
Molecular and cellular biology
Ovarian Neoplasms - enzymology
Ovarian Neoplasms - genetics
Phosphatidylinositol 3-Kinases - metabolism
Protein-Serine-Threonine Kinases
Proto-Oncogene Proteins - metabolism
Proto-Oncogene Proteins c-akt
RNA, Messenger - biosynthesis
RNA, Messenger - genetics
Telomerase - biosynthesis
Telomerase - genetics
Telomerase - metabolism
Transcription, Genetic
Transcriptional Activation
Transfection
Tumor Cells, Cultured
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Telomerase activity is present in >90% of all tumors and appears to be regulated by the phosphatidylinositol 3-kinase signaling pathway. Here we demonstrate that Akt is not involved in the signaling cascade for telomerase regulation in ovarian surface epithelial cells. However, we showed that c-Jun NH2-kinase induces telomerase activity, that inhibition of JNK by JIP abrogates telomerase activity, and that JNK expression activates transcription of a reporter gene fused to the hTERT promoter sequence. Consequently, our data show that JNK is a key regulator of telomerase activity and, hence, may provide new perspectives on tumorigenesis that could be exploited for novel therapeutic strategies.
ISSN:0008-5472
1538-7445