Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/94035
標題: Sirtuin 1 (SIRT1) Deacetylase Activity and NAD⁺/NADH Ratio Are Imperative for Capsaicin-Mediated Programmed Cell Death
作者: Lee, Yi-Hui
Chen, Huei-Yu
Su, Lilly J
Chueh, Pin Ju
關鍵字: apoptosis;autophagy;capsaicin;silent mating type information regulation 1 (sirtuin 1, SIRT1);tumor-associated NADH oxidase (tNOX, ENOX2);Apoptosis;Autophagy;Capsaicin;Cell Line;Cell Line, Tumor;Humans;Lung;NAD;NADH, NADPH Oxidoreductases;RNA Interference;Sirtuin 1
Project: Journal of agricultural and food chemistry, Volume 63, Issue 33, Page(s) 7361-70.
摘要: 
Capsaicin is considered a chemopreventive agent by virtue of its selective antigrowth activity, commonly associated with apoptosis, against cancer cells. However, noncancerous cells possess relatively higher tolerance to capsaicin, although the underlying mechanism for this difference remains unclear. Hence, this study aimed to elucidate the differential effects of capsaicin on cell lines from lung tissues by addressing the signal pathway leading to two types of cell death. In MRC-5 human fetal lung cells, capsaicin augmented silent mating type information regulation 1 (SIRT1) deacetylase activity and the intracellular NAD(+)/NADH ratio, decreasing acetylation of p53 and inducing autophagy. In contrast, capsaicin decreased the intracellular NAD(+)/NADH ratio, possibly through inhibition of tumor-associated NADH oxidase (tNOX), and diminished SIRT1 expression leading to enhanced p53 acetylation and apoptosis. Moreover, SIRT1 depletion by RNA interference attenuated capsaicin-induced apoptosis in A549 cancer cells and autophagy in MRC-5 cells, suggesting a vital role for SIRT1 in capsaicin-mediated cell death. Collectively, these data not only explain the differential cytotoxicity of capsaicin but shed light on the distinct cellular responses to capsaicin in cancerous and noncancerous cell lines.
URI: http://hdl.handle.net/11455/94035
DOI: 10.1021/acs.jafc.5b02876
Appears in Collections:生物醫學研究所

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