Abstract |
In this study, we found that pectenotoxin-2 (PTX-2) decreased cell viability and inhibited telomerase activity with downregulation of hTERT expression in human leukemia cells. PTX-2 treatment also reduced c-Myc and Sp1 gene expression and DNA binding activity. Further chromatin immunoprecipitation assay demonstrated that PTX-2 attenuated the binding of c-Myc and Sp1 to the regulatory regions of hTERT. We also observed that PTX-2 treatment attenuated the phosphorylation of Akt, thereby reducing the phosphorylation and nuclear translocation of hTERT. We concluded that PTX-2 suppressed telomerase activity through the transcriptional and post-translational suppression of hTERT and this process precedes cellular differentiation of human leukemia cells.
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Authors | Mun-Ock Kim, Dong-Oh Moon, Sang-Hyuck Kang, Moon-Soo Heo, Yung Hyun Choi, Jee Hyung Jung, Jae-Dong Lee, Gi-Young Kim |
Journal | FEBS letters
(FEBS Lett)
Vol. 582
Issue 23-24
Pg. 3263-9
(Oct 15 2008)
ISSN: 0014-5793 [Print] England |
PMID | 18775701
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Furans
- Macrolides
- Proto-Oncogene Proteins c-myc
- Pyrans
- Sp1 Transcription Factor
- pectenotoxin 2
- Proto-Oncogene Proteins c-akt
- Telomerase
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Topics |
- Apoptosis
- Cell Line, Tumor
- Cell Proliferation
(drug effects)
- Chromatin Immunoprecipitation
- Furans
(pharmacology)
- Gene Expression
(drug effects)
- Humans
- Leukemia
(metabolism)
- Macrolides
- Phosphorylation
(drug effects)
- Proto-Oncogene Proteins c-akt
- Proto-Oncogene Proteins c-myc
(metabolism)
- Pyrans
(pharmacology)
- Sp1 Transcription Factor
(metabolism)
- Telomerase
(antagonists & inhibitors, genetics)
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