Lipofectin enhances cellular uptake of antisense DNA while inhibiting tumor cell growth.
Lipofectin enhances cellular uptake of antisense DNA while inhibiting tumor cell growth.
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Lipofectin 增强细胞对反义 DNA 的摄取，同时抑制肿瘤细胞生长。
DOI：
10.1089/ard.1992.2.51
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Lynch,MJ
中科院分区：
文献类型：
--
作者：
Yeoman,LC;Danels,YJ;Lynch,MJ
合成一种天然的DNA低聚物（15-mer），其序列与人TGF-α mRNA翻译起始密码子区域互补，并与Lipofectin混合形成单层复合物。结果发现，脂质体- dna低聚物复合物或脂质体单独作用于HCT116细胞均能抑制肿瘤细胞的生长。比较32p标记的15-mers在存在和不存在Lipofectin的情况下进入结肠肿瘤细胞的情况。在接受脂质体与DNA最佳比例的细胞中发现的标记低聚物的数量比单独接受32p标记DNA的细胞中发现的数量高4到10倍。尽管脂质体-反义DNA寡聚物处理HCT116细胞引起了细胞生长的剂量依赖性抑制，但随后目标mRNA产物升高。由于其抑制生长的机制不可能涉及抑制TGF-α的表达，因此我们认为脂脂素可能对细胞膜产生非特异性的、类似清洁剂的作用，从而促进TGF-α的加工和释放。
A natural DNA oligomer (15-mer) was synthesized with a sequence complementary to the translation initiation codon region of the human TGF-α mRNA and mixed with Lipofectin to form unilamellar complexes. It was found that tumor cell growth was inhibited when HCT116 cells were treated with Lipofectin-DNA oligomer complexes or with Lipofectin alone. Uptake of32P-labeled 15-mers into colon tumor cells was compared in the presence and absence of Lipofectin. The amount of labeled oligomer found in cells that received optimal ratios of Lipofectin to DNA was 4- to 10-fold higher than the amount found in cells that received32P-labeled DNA alone. Although Lipofectin—antisense DNA oligomer treatment of HCT116 cells caused a dose-dependent inhibition of cell growth, there was a subsequent rise in target mRNA product. Because the mechanism of growth inhibition could not involve an inhibition of TGF-α expression, it was concluded that Lipofectin probably exerts a nonspecific, detergent-like effect upon the cell membrane, producing an enhancement of TGF-α processing and release.