摘要
目的观察原癌基因N—MYC下游调节基因-2（NDRG2）在不同前列腺癌细胞株中的表达水平和对PC3细胞的体外增殖抑制作用。方法采用逆转录-聚合酶链反应（RT—PCR）及Western blot检测不同前列腺癌细胞株（PC3、LNCaP、DU145）的NDRG2表达水平，使用pAD—CMV腺病毒感染的方法观察NDRG2对PC3细胞的作用，乳糖操纵子z（Lacz）为阳性对照，并设空白对照，噻唑蓝比色法（MTT法）绘制细胞生长曲线、流式细胞仪（FCM）检测感染48、72h的细胞周期及凋亡。结果3个前列腺癌细胞株的NDRG2表达水平相对较低，其中PC3细胞表达水平最低，细胞生长曲线显示NDRG2基因自感染36h开始能够抑制PC3细胞增殖（F≥12．43，P〈0．01），FCM检测发现，感染72h时，包装有NDRG2基因腺病毒感染组同空白及阳性对照组比较，细胞G1期阻滞（3组分别为68．06％、50．33％和50．33％），细胞凋亡增加（3组分别为12．33％、3．21％和3．87％）。结论NDRG2基因可能参与了前列腺癌的发病，腺病毒介导的人NDRG2基因可明显抑制PC3细胞的增殖。
Objective To detect the expression level of N-MYC dwn-stream rgulated gne-2 （NDRG2） in different prostatic carcinoma cell lines, and investigate the inhibitory effects of NDRG2 on proliferation of PC3 cell line mediated by adenovirus in vitro. Methods The expression of NDRG2 mRNA and protein was detected by using RT-PCR and Western blot respectively, pAD_CMV_NDRG2 adenoviruses were used to infect the PC3 cells. The effects of the adenovirus on cell proliferation were observed by using MTT method. The changes in eel1 cycle and apoptosis were detected by flow eytometry at the 48th and 72nd h after the infection. Results The results of RT-PCR and Western blot indicated that the three prostatic carcinoma cell lines had relatively lower NDRG2 mRNA and protein levels. PC3 cells had the lowest level among the three cell lines. MTF method showed that NDRG2 began to suppress the proliferation of the PC3 cells at the 36th h （ F≥ 12.43, P 〈 0.01 ）. Compared with the blank control and the positive control, pAD_CMV_NDRG2-infected cells showed an increase in G1 phase at the 72nd h （68.06% ,50.33% and 50.33% respectively）. Furthermore,NDRG2-indueed apoptosis was also increased at the 72nd h in comparison with the controls （ 12.33% ,3.21% and 3.87% respectively）. Conclusion NDRG2 might be involve in the pathogenesis of the prostatic carcinoma. Adenovirus-mediated NDRG2 could suppress the proliferation of the PC3 ceils significantly.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2009年第10期1275-1277,共3页
Chinese Journal of Experimental Surgery
关键词
前列腺癌
原癌基因
腺病毒
Prostatic carcinoma
Protooncogene
Adenovirus
