平阳霉素诱导舌癌Tca8113细胞凋亡过程中p65信号转导通路的变化

Alternation of p65 transduction pathways during Tca8113 cells apoptosis induced by pingyangmycin

目的观察平阳霉素诱导舌癌T ca8113细胞凋亡过程中p65信号转导通路的动态变化。方法在平阳霉素诱导T ca8113细胞凋亡过程中,流式细胞术检测细胞凋亡,免疫组化、W estern b lot检测p65蛋白。结果平阳霉素能诱导T ca8113细胞凋亡,在凋亡发生时,p65蛋白由非活化状态转变为活化状态,从胞浆中穿过核膜进入细胞核,并调控靶基因表达。调控结束后,p65蛋白由胞核回到胞浆,并成为非活化状态。结论平阳霉素诱导T ca8113细胞凋亡过程中,p65信号转导通路被激活。

Objective： To observe the alteration of p65 signal transduction during Tca8113 cells apoptosis induced by pingyangmycin. Methods： During Tca8113 cells apoptosis induced by pingyangmycin, the apoptosis were observed by flow cytometry and alternation of p65 signal transduction were observed by immunohistochemistry and Western blot analysis. Results： pingyangmycin could induce Tca8113 cells to apoptosis, p65 was activated and translocated into nucleus from cytoplasm during apoptosis, and then regulated the expression of target genes, at last translocated back into cytoplasm and became inactive after the regulation. Conclusion： p65 signal transduction is activated during Tca8113 cells apoptosis induced by pingyangmycin, there may be a correlation between p65 signal transduction and pingyangmycin chemosensitivity.