He Q Y, Zhang H Q, Pang D B, Chi X S, Xue S B
Department of Biology, Beijing Normal University, China.
Zhongguo Yao Li Xue Bao. 1996 Nov;17(6):545-9.
To study the mechanism of resistance to apoptosis in the harringtonine (Har)-resistant HL60 cells with tetrandrine (Tet).
Growth inhibition, flow cytometry, DNA agarose gel electrophoresis, protein phosphorylation, and RNA dot hybridization.
The resistant cells had no cross resistance to Tet. Tet induced the sensitive but not the Har-resistant HL60 cells to apoptosis. The high phosphorylation of protein < 30 kDa occurred when the resistant cells were treated with Tet. Tet and Har increased the expression of c-myc mRNA in the sensitive HL60 cells. The expression of c-myc mRNA in the resistant cells was obviously decreased and almost not changed in treatment with Tet and Har.
Tet induced the sensitive but not the Har-resistant HL60 cells to apoptosis, and the resistance to apoptosis induced by Tet was associated with the high protein phosphorylation and reduction of the expression of c-myc mRNA.
研究粉防己碱(Tet)对高三尖杉酯碱(Har)耐药的HL60细胞抗凋亡机制。
生长抑制、流式细胞术、DNA琼脂糖凝胶电泳、蛋白质磷酸化及RNA斑点杂交。
耐药细胞对Tet无交叉耐药性。Tet诱导敏感的HL60细胞而非Har耐药的HL60细胞凋亡。用Tet处理耐药细胞时出现分子量<30 kDa的蛋白质高度磷酸化。Tet和Har增加敏感HL60细胞中c-myc mRNA的表达。耐药细胞中c-myc mRNA的表达明显降低,用Tet和Har处理时几乎无变化。
Tet诱导敏感的HL60细胞而非Har耐药的HL60细胞凋亡,Tet诱导的抗凋亡作用与蛋白质高度磷酸化及c-myc mRNA表达降低有关。