摘要
目的探讨bcl-2反义寡核苷酸能否增加小细胞肺癌细胞NCI—H69的凋亡。方法将NCI—H69细胞培养传代，细胞共分4组，反义寡核苷酸组、正义寡核苷酸组、无义寡核苷酸组和空白对照组，通过脂质体将不同浓度的寡核苷酸导人细胞中，WesternBlot法检测bcl-2蛋白的表达，流式细胞术检测细胞的凋亡率。结果与空白对照组比较，反义寡核苷酸组的bcl-2蛋白表达明显受到抑制，而正义寡核苷酸组和无义寡核苷酸组细胞的bcl-2蛋白表达则与空白对照组差异不明显。反义寡核苷酸组细胞在10、20、40umol／L 3个不同浓度时的凋亡率分别是（9．97±1．54）％、（15．28±1．73）％、（21．41±1．85）％，明显高于空白组和正义链、无义链组阴性对照组，且差异有统计学意义（F=7．19～15．48，q=5．21—7．98，P〈0．01），而转染正义链和无义链组与空白组比较则差异无统计学意义。结论bcl-2反义寡核苷酸能有效封闭bcl-2基因的表达，增加小细胞肺癌细胞的凋亡。
Objective To study the effect of bcl-2 antisense oligodexynucleotides on the apoptosis in human small-cell lung cancer cell line NCI-H69. Methods Cultured cells were divided into 4 groups： antisense oligodexynucleotides（ASODN）, sense oligodexynucleotides （SODN）, nonsense oligodexynucleotides （NSODN） and control. The different bcl-2 oligodexynucleotides was tmnsfected into corresponding cells using oligofectamine. The expression of bcl-2 was examined by Western blot. The apoptosis rates were measured by flow cytometry （FCM）. Results The bcl-2 expression in ASODN group was significantly inhibited compared to the control group, SODN and NSODN groups, but it was not obviously inhibited in SODN and NSODN groups. The apoptosis rate of ASODN group in different concentration was （9.97±1.54） %, （15.28±1.73） % and （21.41±1.85） % respectively, it was significantly higher than that of the control group （F = 7.19-15.48, q = 5.21-7.98, P 〈0.01）. Conclusion The bcl-2 ASODN could enhance cell apoptosis rate in small-cell lung cancer by blocking bcl-2 gene effectively.
出处
《肿瘤研究与临床》
CAS
2011年第8期515-517,共3页
Cancer Research and Clinic
关键词
基因
bcl-2
癌
小细胞
寡核苷酸类
反义
凋亡
Genes/bcl-2
Carcinoma, small cell
Antisense oligodexynucleotides
Apoptosis
