Bcl-2与c-mycASODN联合转染对裸鼠宫颈癌Hela细胞皮下移植瘤抑制作用研究

Inhibition Effects of Bcl-2 and c-myc Aantisense Oligodeoxynucleotides Combined Transfection on the Human Cervical Cancer Transplanted Subcutaneously in Nude Mice.

目的本研究旨在探讨bcl-2与C-myc反义寡核苷酸（antisenseoligodeoxynucleotides，ASODN）联合转染对人宫颈癌Hela细胞裸鼠皮下移植瘤的抑制作用。方法运用Balb／c裸鼠建立宫颈癌移植瘤模型，随机分成正常对照纽、双基因SODN联合治疗组、bcl-2ASODN纽、c-mycASODN组和双基因ASODN联合治疗组，分别处理后定期测量肿瘤体积，并计算抑瘤率，并在治疗结束后应用缺口末端脱氧核苷酸转移酶标记技术（TUNEL法）检测移植瘤细胞的凋亡。结果25只裸鼠2w后均达成瘤标准，并在治疗第17d后，ASODN组的抑瘤率与对照组、SODN组比较开始有显著性差异（P〈O．01）；治行结束时双基因ASODN组抑瘤率为40.0％，与其他组比较均有统计学意义（P〈0．01）：TUNEL法检测移植瘤细胞凋亡结果显示，高倍镜视野下双基因ASODN组凋亡阳性细胞数为（40.5±4.9）个，与其他组比较有显著性差异（P〈0．01）．结论bcl-2ASODN与c-mycASODN联合治疗比单基因ASODN治疗能更有效的促进人宫颈癌Hela细胞裸鼠皮下移植瘤细胞凋亡、抑制肿瘤生长。

Objective To investigate the inhibition effects of bcl-2 and c-myc ann et al. tisense oligodeoxynucleotides （ASODN） combined transfection on the human cervical cancer transplanted subcutaneously in nude mice. Methods The Hela ceils were cultured and implanted subcutaneously into 25 nude mice .At the 14th day, these mices were divided into five groups： normal control group, bel-2 ＋c-mycSODN group, bcl-2ASODN group, c- mycASODN group and bcl-2＋ c-myc ASODN group. After different treatment, the tmnor volumes were measured and inhibition rate was calculated. Terminal Deoxynueleotidyl Transferase-mediated Nick End Labeling （TUNEL） was used to detect the apoptosis. Results Two weeks after Hela cells implantation, all mice formed solid tumor, and the inhibition rate of ASODN group showed significant difference vs other groups at the 17th day （P〈 0.01 ）. Tile inhibition rate of bcl-2＋c-myc ASODN group was 40.0% at the termination day, and displayed signific, ant difference when compared with other groups （P〈0.01）. The number of apoptosis cells in bcl-2＋c-myc ASODN group was 40.5±4.9 per HPF, there was also significant difference compared with other groups （P〈0.01）. Conclusion Cmnbined genes transfection of the bcl-2ASODN and c-myc ASODN can more effectively inhibit cervical xenografi tumor growth than monogenic transtection via promoting the apopotosis of tumor cell significantly.