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目的：探讨端粒酶（hTERT）基因的两端部分硫代修饰反义核酸（AS PS-ODN）抑制氟他胺耐受型前列腺癌细胞LNCaP端粒酶活性后，肿瘤坏死因子相关凋亡诱导配体（TRAIL）对LNCaP细胞凋亡的增敏作用。方法采用台盼蓝观察hTERT AS PS-ODN与TRAIL共同作用对雄激素非依赖型前列腺癌细胞LNCaP生长活力的影响；倒置显微镜观察凋亡细胞的形态变化；通过双标流式细胞仪测定凋亡细胞的百分率。结果 hTERT AS PS-ODN作用于LNCaP细胞后加入TRAIL100ng/mL作用48h，LNCAP细胞的抑制率与对照组、正义核酸（S PS-ODN）组、AS PS-ODN组、TRAIL组及S PS-ODN+ TRAIL组相比有统计学差异（P＜0.01）。hTERT AS PS-ODN作用于LNCAP细胞后加入TRAIL作用48h，细胞出现典型的凋亡形态变化。hTERT AS PS-ODN作用于LNCaP细胞后加入100ng/mL TRAIL作用48h,凋亡细胞的百分率分别与对照组、S PS-ODN组、AS PS-ODN组、TRAIL组及S PS-ODN+TRAIL组相比有显著性差异（P＜0.05）。结论 hTERT基因反义核酸对TRAIL诱导的氟他胺耐受型前列腺癌细胞LNCaP凋亡有增敏作用。“,”Objective To investigated the effects of telomerase inhibition with hTERT antisense on TRAIL-induced apoptosis in flutamide insensitive prostate cancer cells (LNCaP). Methods Antisense phosphorothioate oligodeoxynucleotide (AS PS-ODN) was synthesized and purified. Cell viability was determined by MTT assay.Cell apoptosis was observed by morphological method and measured by flowcytometry. Results AS PS-ODN could significantly increase TRAIL-induced apoptosis in LNCaP cells. Conclusion Inhibition of telomerase with hTERT antisense can enhance TRAIL-induced apoptosis in flutamide insensitive prostate cancer cells (LNCaP).