Sodium Butyrate Induces Apoptosis in MSN Neuroblastoma Cells in a Calcium Independent Pathway |
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| Authors: | R Rozental R Faharani Y Yu J M Johnson S O Chan F -C Chiu |
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| Institution: | (1) Departments of Cell Biology & Anatomy, Obstetrics and Anesthesiology, New York Medical College, Valhalla, New York 10595, USA;(2) Department of Pediatrics, Albert Einstein College of Medicine, Bronx, New York 10461, USA;(3) Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA, USA;(4) Department of Cell Biology and Anatomy, New York Medical College, BSB room #A21, 95 Grasslands, Valhalla, New York 10595, USA;(5) Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA 30912, USA |
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| Abstract: | Sodium butyrate (NaBt), a histone deacetylase inhibitor, can cause apoptosis in a number of cancer cells. However, the mechanism of this action is poorly understood. Increased intracellular Ca2+] level has been suggested as a likely mechanism, but there is little corroborating data. In this report we provide evidence that NaBt-treated MSN neuroblastoma cells undergo massive apoptosis in the presence of serum and regardless of external or internal Ca2+] levels. Presented data suggest that apoptotic effect of NaBt is both time- and dose-dependent (LD50 1 mM); and that, presence of serum or cAMP, a second messenger molecule that modulates the apoptotic program in a wide variety of cells could not circumvent the apoptotic effect of NaBt. Our findings suggest that NaBt-induced apoptosis in MSN neuroblastoma cells occurs via a pathway that is independent of Ca2+flux, intracellular Ca2+] or cAMP levels. Further, we also present data that exclude a role for PKC or histones acetylation.Special issue dedicated to Lawrence F. Eng |
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| Keywords: | Apoptosis Ca2+ cAMP neuroblastoma sodium butyrate |
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