Matsumoto Goichi, Kushibiki Toshihiro, Kinoshita Yukihiko, Lee Ushaku, Omi Yasushi, Kubota Eiro, Tabata Yasuhiko
Department of Oral and Maxillofacial Surgery, Kanagawa Dental College, 82 Inaoka, Yokosuka, Kanagawa 238-8580, Japan.
Cancer Sci. 2006 Apr;97(4):313-21. doi: 10.1111/j.1349-7006.2006.00174.x.
Double-stranded RNA (dsRNA) plays a major role in RNA interference (RNAi), a process in which segments of dsRNA are initially cleaved by the Dicer into shorter segments (21-23 nt) called small interfering RNA (siRNA). These siRNA then specifically target homologous mRNA molecules causing them to be degraded by cellular ribonucleases. RNAi down regulates endogenous gene expression in mammalian cells. Vascular endothelial growth factor (VEGF) is a key molecule in vasculogenesis as well as in angiogenesis. Tumor growth is an angiogenesis-dependent process, and therapeutic strategies aimed at inhibiting angiogenesis are theoretically attractive. To investigate the feasibility of using siRNA for VEGF in the specific knockdown of VEGF mRNA, thereby inhibiting angiogenesis, we have performed experiments with a DNA vector based on a siRNA system that targets VEGF (siVEGF). It almost completely inhibited the expression of three different isoforms (VEGF120, VEGF164 and VEGF188) of VEGF mRNA and the secretion of VEGF protein in mouse squamous cell carcinoma NRS-1 cells. The siVEGF released from cationized gelatin microspheres suppressed tumor growth in vivo. A marked reduction in vascularity accompanied the inhibition of a siVEGF-transfected tumor. Fluorescent microscopic study showed that the complex of siVEGF with cationized gelatin microspheres was still present around the tumor 10 days after injection, while free siVEGF had vanished by that time. siVEGF gene therapy increased the fraction of vessels covered by pericytes and induced expression of angiopoietin-1 by pericytes. These data suggest that cationized-gelatin microspheres containing siVEGF can be used to normalize tumor vasculature and inhibit tumor growth in a NRS-1 squamous cell carcinoma xenograft model.
双链RNA(dsRNA)在RNA干扰(RNAi)中起主要作用,在该过程中,dsRNA片段最初被Dicer切割成较短的片段(21 - 23个核苷酸),即小干扰RNA(siRNA)。这些siRNA随后特异性靶向同源mRNA分子,导致它们被细胞核糖核酸酶降解。RNAi下调哺乳动物细胞中的内源性基因表达。血管内皮生长因子(VEGF)是血管生成以及血管新生中的关键分子。肿瘤生长是一个依赖血管生成的过程,理论上,旨在抑制血管生成的治疗策略具有吸引力。为了研究使用针对VEGF的siRNA特异性敲低VEGF mRNA从而抑制血管生成的可行性,我们使用了基于靶向VEGF的siRNA系统(siVEGF)的DNA载体进行实验。它几乎完全抑制了小鼠鳞状细胞癌NRS - 1细胞中VEGF mRNA的三种不同异构体(VEGF120、VEGF164和VEGF188)的表达以及VEGF蛋白的分泌。从阳离子化明胶微球释放的siVEGF在体内抑制了肿瘤生长。血管生成的显著减少伴随着siVEGF转染肿瘤的抑制。荧光显微镜研究表明,注射后10天,siVEGF与阳离子化明胶微球的复合物仍存在于肿瘤周围,而游离的siVEGF此时已消失。siVEGF基因治疗增加了被周细胞覆盖的血管比例,并诱导周细胞表达血管生成素 - 1。这些数据表明,含有siVEGF的阳离子化明胶微球可用于使肿瘤血管正常化并抑制NRS - 1鳞状细胞癌异种移植模型中的肿瘤生长。