目的探讨p53凋亡刺激蛋白2(apoptosis stimulating protein 2 of p53,ASPP2)对饥饿诱导的大肠癌HCTll6p53-/-(p53缺失)细胞自噬和凋亡的影响。方法实验分3组:(1)绿色荧光蛋白腺病毒(green fluorescent protein adenovirus,rAd-GFP)感染组(对照组);(2)自噬抑制剂LY294002处理组;(3)ASPP2腺病毒(ASPP2adenovirus,rAd-ASPP2)感染组。无血清培养基分别培养0、24、48h诱导细胞自噬和凋亡。利用calcein/PI吸收试验观察各组细胞凋亡水平。细胞转染红色荧光蛋白自噬质粒Lc3(cerisefluorescentproteinautophagyplasmidLc3,CFP-Lc3),在荧光显微镜下观察各组细胞自噬水平。结果rAd—GFP感染组饥饿24h细胞的自噬水平升高显著(0h:1.04±0.24;24h:12.17±0.86,P〈0.05),而凋亡水平改变差异无统计学意义(0h:2.01%4-0.06%;24h:3.23%±0.34%,P〉0.05);饥饿时间延长至48h,自噬水平(0h:1.044-0.24;48h:21.094-3.32)和凋亡水平(0h:2.01%4-0.06%;48h:30.20%-I-3.18%)升高,差异均具有统计学意义(均P〈0.05)。使用LY294002抑制细胞自噬,饥饿24h细胞凋亡显著增多(rAd—GFP组:3.23%±0.34%;LY294002组:15.68%±1.24%,P〈0.01),而饥饿48h凋亡显著减少(rAd—GFP组:30.20%±3.18%;LY294002组:25.44%4-3.01%,P〈0.05)。rAd—ASPP2感染组饥饿24h自噬显著降低(rAd.GFP组:12.17±0.86;ASPP2组:1.454-0.45,P〈0.01),而凋亡显著升高(rAd—GFP组:3.23%±0.34%;ASPP2组:10.45%±0.81%,P〈0.05);饥饿48h自噬(rAd—GFP组:21.09±3.32;ASPP2组:29.93±3.48)和凋亡(rAd.GFP组:30.20%±3.18%;ASPP2组:36.72%±2.74%)水平均显著升高(均P〈0.05)。结论ASPP2通过对自噬的双向调节促进饥饿诱导的大肠癌HCTl16p53。一细胞凋亡。