Rha S Y, Noh S H, Kwak H J, Wellstein A, Kim J H, Roh J K, Min J S, Kim B S, Chung H C
Yonsei Cancer Research Institute, Yonsei University College of Medicine, Seoul, South Korea.
Cancer Lett. 1997 Sep 16;118(1):37-46. doi: 10.1016/s0304-3835(97)00215-2.
We studied biological phenotypes of gastric cancer cell lines based on a novel heparin-binding growth/differentiation factor (midkine (MK)) expression. MK expression was found in 67% (6/9) of the gastric cancer cell lines and 56% (14/25) of the primary cancer tissues. Gastric cancer cell lines with MK expression showed higher colony forming activity in soft agar assay and endothelial cell growth stimulatory effect in cross-feeding assay than cells which did not express MK. However, urokinase-type plasminogen activator (uPA) expression and tumor invasiveness did not correlate with MK expression. Growth of MK expressing cells was inhibited by a heparin-binding blocking agent, pentosan polysulfate (PPS). In cancer tissues, MK expression correlated with tumor size, suggesting in vivo autocrine and paracrine activity. This proliferation promoting activity of MK can be targeted by an anti-heparin binding agent as a biotherapy model in gastric cancer.
我们基于一种新型肝素结合生长/分化因子（中期因子（MK））的表达，研究了胃癌细胞系的生物学表型。在67%（6/9）的胃癌细胞系和56%（14/25）的原发性癌组织中发现了MK表达。与未表达MK的细胞相比，表达MK的胃癌细胞系在软琼脂试验中显示出更高的集落形成活性，在交叉喂养试验中显示出对内皮细胞生长的刺激作用。然而，尿激酶型纤溶酶原激活剂（uPA）的表达和肿瘤侵袭性与MK表达无关。表达MK的细胞的生长受到肝素结合阻断剂戊聚糖多硫酸盐（PPS）的抑制。在癌组织中，MK表达与肿瘤大小相关，提示其在体内的自分泌和旁分泌活性。作为胃癌生物治疗模型，MK的这种增殖促进活性可被抗肝素结合剂靶向作用。
