Nagashima A, Yasumoto K, Nakahashi H, Furukawa T, Inokuchi K, Nomoto K
Cancer Res. 1986 Sep;46(9):4420-4.
High- (Cl-33H) and low- (Cl-35L) metastatic clones were established from a methylcholanthrene-induced rat fibrosarcoma (FMQ-100). The modal chromosome numbers of the two clones were different. These clones grew in in vitro culture, showing similar growth rate and saturation density. However, in in vivo experiments, Cl-33H exhibited a higher tumor growth rate, tumorigenicity, spontaneous metastatic potential, and experimental metastatic potential than did Cl-35L. Alveolar macrophages obtained from normal syngeneic rats stimulated growth of these clones in vitro, as assessed by [3H]thymidine uptake. Moreover, this effect was greater on Cl-33H than Cl-35L. The growth-promoting effect of macrophages was also observed under the in vitro condition of lack of direct contact between macrophages and tumor cells. These results suggested the possibility that alveolar macrophage-derived growth-promoting factors play some role in the development of pulmonary metastasis in this tumor system, and the difference of susceptibility to the growth-promoting factors might be one of the causes of the different metastatic potentials of Cl-33H and Cl-35L.
从甲基胆蒽诱导的大鼠纤维肉瘤(FMQ - 100)中建立了高转移(Cl - 33H)和低转移(Cl - 35L)克隆。这两个克隆的众数染色体数不同。这些克隆在体外培养中生长,显示出相似的生长速率和饱和密度。然而,在体内实验中,Cl - 33H比Cl - 35L表现出更高的肿瘤生长速率、致瘤性、自发转移潜能和实验性转移潜能。通过[3H]胸苷摄取评估,从同基因正常大鼠获得的肺泡巨噬细胞在体外刺激了这些克隆的生长。此外,这种作用对Cl - 33H的影响比对Cl - 35L的影响更大。在巨噬细胞与肿瘤细胞缺乏直接接触的体外条件下也观察到了巨噬细胞的促生长作用。这些结果提示,肺泡巨噬细胞衍生的促生长因子可能在该肿瘤系统的肺转移发展中起一定作用,对促生长因子敏感性的差异可能是Cl - 33H和Cl - 35L转移潜能不同的原因之一。