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http://dx.doi.org/10.5352/JLS.2009.19.2.157

Inhibition of Apoptosis by Nitric Oxide in MCF-7 Cells  

Kim, Kyun-Ha (Department of Biology, College of Natural Sciences, Pusan National University)
Roh, Sang-Geun (Department of Biology, College of Natural Sciences, Pusan National University)
Park, Hae-Ryun (Department of oral pathology, College of Dentistry, Pusan National University)
Choi, Won-Chul (Department of Biology, College of Natural Sciences, Pusan National University)
Publication Information
Journal of Life Science / v.19, no.2, 2009 , pp. 157-162 More about this Journal
Abstract
Nitric oxide (NO) is a diffusible, multifunctional and transcellular messenger that has been implicated in numerous physiological and pathological conditions. It has been reported that NO induced apoptosis in tumor cells, macrophage cells and inhibited apoptosis in normal cells, endothelial cells. To examine whether NO could induce apoptosis in MCF-7 cells, cells were treated with SIN-1 (3-morpholinosydnonimine), NO donor. Cell viability did not change in SIN-1 treated cells for 48 h and there was no significantly changes in cell cycle progression or growth pattern by FACS analysis. But p53 protein, an apoptosis-related factor, increased SIN-1 treatment time dependently. Bcl-2, MDM2 and p21 were also accumulated. Bax level did not change. A major role of inhibiting apoptosis by NO in MCF-7 cells, cobalt chloride ($CoCl_2$) was added to cells preincubated with SIN-1. Whereas $CoCl_2$ treated cells underwent apoptosis, for 24 h SIN-1 preincubated cells were not induced apoptosis. Inactivated proteins, MDM2 and bcl-2, by $CoCl_2$ levels also increased in SIN-1 pre-treated cells. These results suggested that SIN-1 blocked p53 by MDM2 activation and inhibited apoptosis by inducing p21 and bcl-2 expression.
Keywords
MCF-7; Nitric oxide; p53; MDM2; bcl-2;
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