Merlin Represses Ras-Induced Cyclin D1 Transcription through the Cyclic AMP-Responsive Element
The Korean Journal of Physiology and Pharmacology
;
: 289-293, 2003.
Article
in English
| WPRIM
| ID: wpr-727403
ABSTRACT
Mutations in the NF2 tumor suppressor gene cause neurofibromatosis type 2, an autosomal dominant inherited syndrome predisposed to the multiple tumors of the nervous system. Merlin, the NF2 gene product was reported to block Ras-mediated cell transformation and represses Ras-induced expression of cyclin D1. However, the potential mechanism underlying the anti-Ras function of merlin on the cyclin D1 is still unclear. In this study, we investigated whether merlin decreases Ha-ras-induced accumulation of cyclin D1 at the transcriptional level, and demonstrated that merlin suppressed Ras-induced cyclin D1 promoter activity mediated by the cyclic AMP-responsive element (CRE) in SK-N-BE (2) C neuroblastoma cells. Furthermore, we found that merlin attenuated active Ras and forskolin-induced CRE-driven promoter activity. These results suggest that the transcriptional repression of the cyclin D1 expression by merlin may contribute to the inhibition of Ras-induced cell proliferation
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Repression, Psychology
/
Genes, Tumor Suppressor
/
Neurofibromatosis 2
/
Cyclins
/
Cyclin D1
/
Neurofibromin 2
/
Cell Proliferation
/
Nervous System Neoplasms
/
Neuroblastoma
Language:
English
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
2003
Type:
Article
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