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Pectenotoxin-2 represses telomerase activity in human leukemia cells through suppression of hTERT gene expression and Akt-dependent hTERT phosphorylation.

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.
AuthorsMun-Ock Kim, Dong-Oh Moon, Sang-Hyuck Kang, Moon-Soo Heo, Yung Hyun Choi, Jee Hyung Jung, Jae-Dong Lee, Gi-Young Kim
JournalFEBS letters (FEBS Lett) Vol. 582 Issue 23-24 Pg. 3263-9 (Oct 15 2008) ISSN: 0014-5793 [Print] England
PMID18775701 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Furans
  • Macrolides
  • Proto-Oncogene Proteins c-myc
  • Pyrans
  • Sp1 Transcription Factor
  • pectenotoxin 2
  • Proto-Oncogene Proteins c-akt
  • Telomerase
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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