治疗去势抵抗性前列腺癌（CRPC）的一种有前途的从头方法利用细胞介导的酶前药疗法，包括胞嘧啶脱氨酶（CD）和氟尿嘧啶（5-FC）。本研究的目的是确定细菌 CD 过表达 hTERT 永生化人脂肪干细胞 (hTERT-ADSC.CD) 抑制 CRPC 的潜力。使用编码细菌CD基因的慢病毒载体转染并产生hTERT-ADSC.CD系。在体外研究了细胞选择性迁移至恶性细胞的能力。 PC3和hTERT-ADSC.CD细胞共培养。分别通过心内和皮下注射hTERT-ADSC.CD和1×106 PC3细胞给裸鼠，并给予5-FC 14天。 hTERT-ADSC.CD 已成功设计。给予 5 μM 5-FC 后，体外 hTERT-ADSC.CD 细胞毒性和自杀效应明显增强。 hTERT-ADSC.CD 与 5-FC 一起增加了发生凋亡的 PC3 细胞的数量。与给予hTERT-ADSC.CD单一疗法的对照相比，hTERT-ADSC.CD与5-FC组合显示出对肿瘤更大的抑制作用。在携带 CPRC 的小鼠中，CD 过表达的 ADSC 和前药 5-FC 的组合增强了肿瘤抑制作用。表现出 CD 基因表达的干细胞是治疗 CRPC 的一种潜在的新方法。

A promising de novo approach for the treatment of Castration-resistant prostate cancer (CRPC) exploits cell-mediated enzyme prodrug therapy comprising cytosine deaminase (CD) and fluorouracil (5-FC). The aim of this study was to determine the potential of bacterial CD-overexpressing hTERT-immortalized human adipose stem cells (hTERT-ADSC.CD) to suppress CRPC. A lentiviral vector encoding a bacterial CD gene was used to transfect and to generate the hTERT-ADSC.CD line. The ability of the cells to migrate selectively towards malignant cells was investigated in vitro. PC3 and hTERT-ADSC.CD cells were co-cultured. hTERT-ADSC.CD and 1 × 106 PC3 cells were administered to nude mice via intracardiac and subcutaneous injections, respectively, and 5-FC was given for 14 days. hTERT-ADSC.CD were successfully engineered. Enhanced in vitro hTERT-ADSC.CD cytotoxicity and suicide effect were evident following administration of 5 μM 5-FC. hTERT-ADSC.CD, together with 5-FC, augmented the numbers of PC3 cells undergoing apoptosis. In comparison to controls administered hTERT-ADSC.CD monotherapy, hTERT-ADSC.CD in combination with 5-FC demonstrated a greater suppressive effect on tumor. In CPRC-bearing mice, tumor suppression was enhanced by the combination of CD-overexpressing ADSC and the prodrug 5-FC. Stem cells exhibiting CD gene expression are a potential novel approach to treatment for CRPC.