Marchetti C, Migliorati G, Moraca R, Riccardi C, Nicoletti I, Fabiani R, Mastrandrea V, Morozzi G
Department of Cell and Molecular Biology, University of Perugia, Italy.
Cancer Lett. 1997 Mar 19;114(1-2):97-9. doi: 10.1016/s0304-3835(97)04634-x.
Short chain fatty acids (propionate and butyrate) and deoxycholic acid (DCA) are able to induce apoptosis in HT-29 colonic tumor cell line, but DCA induces a much higher level of apoptosis than butyrate and propionate. Mixtures of DCA with butyrate or propionate enhance the effect of the single components. Apoptosis is not affected by the PKC, PTK or de novo mRNA and protein synthesis inhibitors, so that the involvement of these enzymes and processes is ruled out. In contrast, DCA-induced apoptosis is directly related to [Ca2+]i concentration as demonstrated by the apoptosis inhibition caused by [Ca2+]i chelator BAPTA/AM.
短链脂肪酸(丙酸和丁酸)以及脱氧胆酸(DCA)能够诱导HT - 29结肠肿瘤细胞系发生凋亡,但DCA诱导的凋亡水平比丁酸和丙酸高得多。DCA与丁酸或丙酸的混合物可增强单一成分的作用效果。凋亡不受蛋白激酶C(PKC)、蛋白酪氨酸激酶(PTK)或从头mRNA和蛋白质合成抑制剂的影响,因此排除了这些酶和过程的参与。相反,如钙离子(Ca2+)螯合剂BAPTA/AM所引起的凋亡抑制所示,DCA诱导的凋亡与细胞内钙离子浓度([Ca2+]i)直接相关。