Buerkle M A, Pahernik S A, Sutter A, Jonczyk A, Messmer K, Dellian M
Institute for Surgical Research, Klinikum Grosshadern, Marchioninistrasse 15, Ludwig-Maximilians-University, 81377 Munich, Germany.
Br J Cancer. 2002 Mar 4;86(5):788-95. doi: 10.1038/sj.bjc.6600141.
Anti-angiogenetic cancer therapy is a potential new form for treatment of solid tumours. The alpha(v)-integrins (alpha(v)beta3, alpha(v)beta5) mediate the contact of activated endothelial cells to proteins of the extracellular matrix during tumour angiogenesis as a prerequisite for survival of endothelial cells. The aim of this study was to investigate the effects of application of a methylated cyclic RGD-peptide as an alpha(v)-integrin antagonist on angiogenesis, microcirculation, growth and metastasis formation of a solid tumour in vivo. Experiments were performed in the dorsal skinfold preparation of Syrian Golden hamsters bearing the amelanotic hamster melanoma A-Mel-3. Animals were injected intraperitoneally with a methylated cyclic RGD-peptide every 12 h, the control group received an inactive peptide. Microcirculatory parameters of tumour angiogenesis including functional vessel density, red blood cell velocity, vessel diameter and leucocyte-endothelium interaction were analysed using intravital microscopy. In an additional study the effects on growth and metastasis of subcutaneous A-Mel-3 were quantified. Functional vessel density was markedly reduced on day 3 in treated animals compared to controls (37.2 +/- 12.1 vs 105.2 +/- 11.2 cm(-1); mean +/- s.e.m.; P<0.05) and increased subsequently in both groups. Red blood cell velocity at day 3 was below values of controls (0.026 +/- 0.01 vs 0.12 +/- 0.03 mm x s(-1); P<0.05). No differences were observed in vessel diameters and leucocyte-endothelium interaction was almost absent in both groups. Furthermore, growth and metastasis of subcutaneous tumours after administration of the cyclic RGD-peptide was significantly delayed in comparison to controls (P<0.05). Inhibition of alpha(v)-integrins by a cyclic RGD-peptide resulted in significant reduction of functional vessel density, retardation of tumour growth and metastasis in vivo. Taken together, these results implicate RGD-peptides as agents which have anti-tumour and anti-metastatic activity in vivo.
抗血管生成癌症治疗是一种治疗实体瘤的潜在新方法。α(v)整合素(α(v)β3、α(v)β5)在肿瘤血管生成过程中介导活化的内皮细胞与细胞外基质蛋白的接触,这是内皮细胞存活的前提条件。本研究的目的是探讨应用甲基化环RGD肽作为α(v)整合素拮抗剂对体内实体瘤血管生成、微循环、生长和转移形成的影响。实验在携带无黑色素仓鼠黑色素瘤A-Mel-3的叙利亚金仓鼠背部皮褶制备物中进行。动物每12小时腹腔注射一次甲基化环RGD肽,对照组接受无活性肽。使用活体显微镜分析肿瘤血管生成的微循环参数,包括功能性血管密度、红细胞速度、血管直径和白细胞-内皮细胞相互作用。在另一项研究中,对皮下A-Mel-3的生长和转移影响进行了量化。与对照组相比,治疗动物在第3天的功能性血管密度显著降低(37.2±12.1对105.2±11.2 cm(-1);平均值±标准误;P<0.05),随后两组均升高。第3天的红细胞速度低于对照组值(0.026±0.01对0.12±0.03 mm×s(-1);P<0.05)。两组在血管直径上未观察到差异,且白细胞-内皮细胞相互作用在两组中几乎不存在。此外,与对照组相比,给予环RGD肽后皮下肿瘤的生长和转移明显延迟(P<0.05)。环RGD肽抑制α(v)整合素导致体内功能性血管密度显著降低、肿瘤生长和转移延迟。综上所述,这些结果表明RGD肽在体内具有抗肿瘤和抗转移活性。