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Pectenotoxin-2 induces G2/M phase cell cycle arrest in human breast cancer cells via ATM and Chk1/2-mediated phosphorylation of cdc25C.

Authors
  • Moon, Dong-Oh
  • Kim, Mun-Ock
  • Nam, Taek-Jeong
  • Kim, Se-Kwon
  • Choi, Yung Hyun
  • Kim, Gi-Young
Type
Published Article
Journal
Oncology Reports
Publisher
Spandidos Publications
Publication Date
Jul 01, 2010
Volume
24
Issue
1
Pages
271–276
Identifiers
PMID: 20514472
Source
Medline
License
Unknown

Abstract

Although pectenotoxin-2 (PTX-2) is known to regulate the actin depolymerization and to induce apoptosis through downregulation of telomerase activity, little is known on its effect on the cell cycle regulation. Therefore, we investigated the effects of PTX-2 on G2/M arrest in human breast cancer cells (MDA-MB-231 and MCF-7). Treatment with PTX-2 significantly suppressed cell proliferation and induced G2/M phase arrest through down-regulation of cyclin B1 and cdc2 expression, but also through phosphorylation of cdc25C. We found increased phosphorylation of ATM and Chk1/2 in a PTX-2 dose-dependent manner. Furthermore, treatment with PTX-2 increased H2O2 generation with correlated G2/M arrest. Our results showed that ATM- and Chk1/2-mediated phosphorylation of cdc25C plays a major role in G2/M arrest, but not in H2O2 generation induced by PTX-2 treatment. We also observed that PTX-2-induced cell cycle arrest was not restricted to p53 status in human breast cancer cells.

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