Zhang Lei, Gasper Warren J, Stass Sanford A, Ioffe Olga B, Davis Myrtle A, Mixson A James
Department of Pathology, University of Maryland Baltimore, Baltimore, Maryland 21201, USA.
Cancer Res. 2002 Oct 1;62(19):5463-9.
The vascular endothelial growth factor receptor (VEGFR) is an important angiogenic target for cancer gene therapy. In this study, we designed an mRNA-cleaving oligodeoxynucleotide that targets the VEGF receptor 2 (VEGFR2) transcript (VEGFR2 DNAzyme). This DNAzyme was found to digest efficiently mRNA substrates of VEGFR2 in a concentration- and time-dependent manner. We also showed that the DNAzyme induces apoptosis and markedly inhibits endothelial cell growth compared with a disabled DNAzyme and untreated controls. In contrast, the DNAzyme did not inhibit the growth of MDA-MB-435 cells in vitro. The DNAzyme in complex with a nonviral carrier also significantly inhibited tumor growth in vivo. After the fourth injection, there was nearly a 75% reduction of tumor size in the DNAzyme-treated group compared with the saline-injected control group (P = 0.024). Marked cell death in the peripheral regions of the tumor accompanied by a reduction in blood vessel density is consistent with the antiangiogenic mechanism of the DNAzyme. This study indicates that DNAzymes, targeting angiogenic growth factors of tumors, show promise as antitumor agents.
血管内皮生长因子受体(VEGFR)是癌症基因治疗的一个重要血管生成靶点。在本研究中,我们设计了一种靶向血管内皮生长因子受体2(VEGFR2)转录本的mRNA切割寡脱氧核苷酸(VEGFR2脱氧核酶)。发现这种脱氧核酶能以浓度和时间依赖的方式有效消化VEGFR2的mRNA底物。我们还表明,与失活的脱氧核酶和未处理的对照相比,该脱氧核酶可诱导细胞凋亡并显著抑制内皮细胞生长。相反,该脱氧核酶在体外不抑制MDA-MB-435细胞的生长。与非病毒载体复合的脱氧核酶在体内也显著抑制肿瘤生长。第四次注射后,与注射生理盐水的对照组相比,脱氧核酶治疗组的肿瘤大小减少了近75%(P = 0.024)。肿瘤周边区域明显的细胞死亡伴随着血管密度的降低,这与脱氧核酶的抗血管生成机制一致。本研究表明,靶向肿瘤血管生成生长因子的脱氧核酶有望成为抗肿瘤药物。