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In vitro effects of 2‐methoxyestradiol on cell morphology and Cdc2 Kinase activity in SNO oesophageal carcinoma cells
Author(s) -
Joubert Annie,
Marais Sumari
Publication year - 2007
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1409
Subject(s) - apoptosis , mitosis , cyclin dependent kinase 1 , metaphase , kinase , cell cycle , microbiology and biotechnology , cell growth , in vitro , cell , biology , chemistry , cancer research , biochemistry , gene , chromosome
The effects of 1 × 10 −6 M exogenous 2‐methoxyestradiol (2 ME) were determined on cell morphology and cell division cycle (Cdc) 2 kinase activity in SNO oesophageal carcinoma cells. Mitotic indices revealed an increase in metaphase cells (11.2%) when compared to the 0.5% vehicle‐treated cells after 18 h of exposure to 2 ME. Vehicle‐treated control cells did not show any hallmarks of apoptosis after 18 h of exposure to dimethyl sulphoxide. Only 0.5% of 2 ME‐treated cells showed characteristics of apoptosis. Conversely, increased morphological hallmarks of apoptosis were observed in SNO‐treated cells after 21.5 h of 2 ME exposure. When compared to the 0.5% in vehicle‐treated cells, 4.7% of cells were in apoptosis. Furthermore, 34.1% of cells were blocked in metaphase after 21.5 h of 2 ME exposure compared to 0.6% of vehicle‐control cells. In addition, Cdc2 kinase activity was statistically significantly increased (1.3‐fold) ( p < 0.005) in 2 ME‐treated cells when compared to vehicle‐treated controls. The present preliminary study suggests that the accumulation observed in metaphase cells and the increase in Cdc2 kinase activity caused by 2 ME are consistent with morphological hallmarks of mitotic arrest and disrupted mitotic spindle formation, thus leading to induction of apoptosis in SNO cells. Copyright © 2007 John Wiley & Sons, Ltd.