中文摘要：

【目的】明确糖酵解调节基因PFKFB3参与11-脱氧轮枝菌素A（11′deoxyverticillinA，C42）诱导HeLa细胞自噬和凋亡中的作用。【方法】利用电镜、荧光显微镜、蛋白免疫杂交、转染、MTS活性检测、siRNA干扰、定量RT-PCR等对C42处理的HeLa细胞自噬和凋亡情况进行了检测。【结果】C42能够引起HeLa细胞不同的死亡。敲降白噬关键基因BECNl或LC3后，明显增加PARP-1的切割和促进C42引起的细胞活性丢失。尽管高浓度C42能更明显地抑制细胞增殖，但却不能增加细胞的自噬流；C42促进的自噬能被糖酵解调节基因PFKFB3的抑制剂所降低；而过量表达糖酵解调节基因PF尉啊3能促进细胞自噬。【结论】糖酵解调节基因PFKFB3直接参与了C42诱导的HeLa细胞自噬，这种自噬的发生抑制了其诱导的细胞凋亡。

英文摘要：

[ Objective ] The aim is to reveal the role of PFKFB3 in 11′-deoxyverticillin A （C42） -induced autophagy and apoptosis. [Methods] Electron and fluorescence microscopy, immunoblotting, MTS assay, siRNA interference and real time PCR were used. [ Results] C42 could induce multiple cell death in HeLa cells. Knockdown of either Beclin 1 or LC3, two important autophagic genes, increased both PARP-1 cleavage and cell viability loss. Although high dose of C42 triggered more cell viability loss, yet, it failed to augment autophagic flux. While PFKFB3 inhibitors attenuated C42- induced autophagy, the overexpression of PFKFB3 increased the induced autophagic flux. [ Conclusion] PFKFB3 is involved in C42 induced-autophagy, which blunts the caspase-dependent apoptotic process.