Sodium butyrate induces apoptosis in MSN neuroblastoma cells in a calcium independent pathway
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 [Ca(2+)] level has been suggested as a likely mechanism, but there is little corroborating data. In this repor...
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| Veröffentlicht in: | Neurochemical research 2004-11, Vol.29 (11), p.2125-2134 |
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| container_title | Neurochemical research |
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| creator | Rozental, R Faharani, R Yu, Y Johnson, J M Chan, S O Chiu, F C |
| description | 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 [Ca(2+)] 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 [Ca(2+)] 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 Ca(2+) flux, intracellular [Ca(2+)] or cAMP levels. Further, we also present data that exclude a role for PKC or histones acetylation. |
| doi_str_mv | 10.1007/s11064-004-6886-9 |
| format | Article |
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However, the mechanism of this action is poorly understood. Increased intracellular [Ca(2+)] 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 [Ca(2+)] 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 Ca(2+) flux, intracellular [Ca(2+)] or cAMP levels. 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However, the mechanism of this action is poorly understood. Increased intracellular [Ca(2+)] 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 [Ca(2+)] 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 Ca(2+) flux, intracellular [Ca(2+)] or cAMP levels. 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| subjects | Apoptosis - drug effects Brain Neoplasms - pathology Bucladesine - pharmacology Butyrates - pharmacology Calcium - metabolism Calcium - pharmacology Calcium Signaling - drug effects Calcium Signaling - physiology Cell Line, Tumor DNA Fragmentation Humans Neuroblastoma - pathology Phosphodiesterase Inhibitors - pharmacology Tetrazolium Salts Theophylline - pharmacology Thiazoles |
| title | Sodium butyrate induces apoptosis in MSN neuroblastoma cells in a calcium independent pathway |
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