Saiki I
Research Institute for Wakan-yaku, Toyama Medical and Pharmaceutical University, Japan.
Jpn J Pharmacol. 1997 Nov;75(3):215-42. doi: 10.1254/jjp.75.215.
The adhesive interaction between tumor cells and host cells or the extracellular matrix plays a crucial role in metastasis formation. Therefore, understanding the mechanism controlling metastasis may assist in the development of antimetastatic therapy. We have used synthetic or recombinant polypeptide analogues containing the Arg-Gly-Asp (RGD) sequence found in the functional domains of fibronectin, such as poly(RGD) or CH-271, to regulate the mechanisms involved in cell adhesion during the metastatic process. Poly(RGD) inhibited experimental lung and liver metastasis effectively when coinjected i.v. with various types of tumors. In a model of spontaneous lung metastasis using the B16-BL6 melanoma, repeated administration of this polypeptide before or after surgical excision of the primary tumor resulted in a significant inhibition of tumor metastasis without affecting the growth of the primary tumor and substantially prolonged the survival time of mice. The mechanism responsible for the inhibition of tumor metastasis by the polypeptides is at least partly associated with the ability to interfere with cellular functions such as adhesiveness, motility and invasiveness in the process of metastasis. Combined treatment of the CH-271 fusion polypeptide and anticancer drugs, i.e., anti-adhesion therapy combined with chemotherapy, caused a marked inhibition of lung and liver metastasis of tumors as compared with either treatment alone or with the control. In contrast, the promotion of tumor cell interaction with immune cells via cell adhesion molecules, which differs from the anti-adhesive mechanism, may lead to the induction of anti-tumor immune responses and, consequently, to the inhibition of tumor metastasis. The transfection of the gene of the B7-1 adhesion molecule into tumor cells (B16-BL6 or K1735-M2 melanoma) resulted in the remarkable reduction of lung metastasis caused by the i.v. injection into mice. Immunization of B7-transfected tumor was effective as a tumor vaccine for preventing the metastasis of B7 negative original tumor cells. Thus, the regulation of the adhesive interaction with tumor cells may provide a new and promising approach for the control and prevention of cancer metastasis.
肿瘤细胞与宿主细胞或细胞外基质之间的黏附相互作用在转移形成过程中起着关键作用。因此,了解控制转移的机制可能有助于抗转移治疗的发展。我们使用了含有在纤连蛋白功能域中发现的精氨酸 - 甘氨酸 - 天冬氨酸(RGD)序列的合成或重组多肽类似物,如聚(RGD)或CH - 271,来调节转移过程中涉及细胞黏附的机制。当与各种类型的肿瘤静脉内共同注射时,聚(RGD)有效地抑制了实验性肺和肝转移。在使用B16 - BL6黑色素瘤的自发性肺转移模型中,在原发性肿瘤手术切除之前或之后重复给予这种多肽导致肿瘤转移的显著抑制,而不影响原发性肿瘤的生长,并显著延长了小鼠的存活时间。多肽抑制肿瘤转移的机制至少部分与在转移过程中干扰细胞功能如黏附性、运动性和侵袭性的能力有关。与单独治疗或对照相比,CH - 271融合多肽与抗癌药物的联合治疗,即抗黏附治疗与化疗联合,对肿瘤的肺和肝转移产生了显著抑制。相反,通过细胞黏附分子促进肿瘤细胞与免疫细胞的相互作用,这与抗黏附机制不同,可能导致抗肿瘤免疫反应的诱导,从而抑制肿瘤转移。将B7 - 1黏附分子基因转染到肿瘤细胞(B16 - BL6或K1735 - M2黑色素瘤)中导致静脉内注射到小鼠体内引起的肺转移显著减少。用B7转染的肿瘤进行免疫作为一种肿瘤疫苗可有效预防B7阴性原始肿瘤细胞的转移。因此,调节与肿瘤细胞的黏附相互作用可能为控制和预防癌症转移提供一种新的、有前景的方法。