期刊文献+

c-erbB-2反义寡核苷酸对人卵巢癌SKOV_3细胞增殖的抑制作用 被引量:1

Inhibitory Effects of c-erbB-2 Antisense Oligodeoxynucleotides Transfection on the Human Ovarian Carcinoma SKOV_3 Cell Lines
下载PDF
导出
摘要 目的探讨c-erbB-2基因反义寡核苷酸转染对人卵巢癌SKOV3细胞增殖的抑制作用及其分子机制。方法实验分空白对照组、正常对照组、c-erbB-2正义对照组及c-erbB-2反义治疗组。脂质体转染后不同时间分别进行MTT试验、集落形成试验、荧光显微镜检测、蛋白质荧光强度测定,以观察不同条件处理后各组细胞的增殖、凋亡、蛋白质表达有无差别。结果反义治疗组与正义对照组比较:转染72hOD值分别为0.201与1.298(P<0.01);克隆形成率分别为26.5%与76.5%(P<0.05);凋亡率分别为21.3%与7.5%(P<0.05),同时明显地下调c-erbB-2蛋白质的表达水平(P<0.05)。结论在卵巢癌的基因治疗中,c-erbB-2反义寡核苷酸能明显抑制人卵巢癌SKOV3细胞的增殖。 Objective To investigate the proliferating inhibition and the mechanisms of c-erbB-2 antisense oligodeoxynucleotides(ASODN) transfection on the human ovarian carcinoma SKOV3 cell lines. Methods There were 4 groups in our study, blank control group, normal control group, c-erbB-2 sense control group and c-erbB-2 antisense experimental group. In the different time after liposome-mediated transfection, the cell proliferation, apoptosis, protein expressing level were observed by MTT assay, flow cytometry,fluorescent microscope and cloning test. Results According to the c-erbB-2 antisense experimental group and the c-erbB-2 sense control group,the OD-value were 0. 201 and 1. 298(P〈0.01) respectively 72h after transfected; the cloning efficiency were 26.5 % and 76.5 % (P〈0. 05)respectively; the apoptosis rate were 21.3% and 7. 5^(P〈0. 05)respectively;and the level of P185 protein was decreased statisti cally in ASODN group, respectively. Conclusion The study suggested that the proliferation of the human ovarian carcinoma SKOV3 cell lines can be inhibited by the c erbB-2 ASODN.
出处 《肿瘤防治研究》 CAS CSCD 北大核心 2006年第10期707-709,共3页 Cancer Research on Prevention and Treatment
基金 国家自然科学基金资助项目(30070230)
关键词 SKOV3细胞 反义寡核苷酸 卵巢癌 C-ERBB-2基因 SKOV3cell lines Antisense oligodeoxynucleotides Ovarian carcinoma c-erbB-2 gene
  • 相关文献

参考文献2

二级参考文献4

  • 1金志军,中华妇产科杂志,1995年,30卷,222页
  • 2杨静平,生物化学与生物物理学报,1993年,25卷,231页
  • 3吴令英,中华妇产科杂志,1996年,31卷,3期,168页
  • 4宋海峰,汤仲明.反义药物作用中的“靶二级结构域”[J].药学学报,2001,36(8):585-589. 被引量:5

共引文献20

同被引文献5

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部