• 1 January 1983
    • journal article
    • research article
    • Vol. 43  (8) , 3754-3758
Abstract
Cellular growth interactions were studied between neonatal human lung fibroblasts (NLF-13) and human tumor lines derived from carcinomas of the prostate (PC-3, DU145), bladder (J82), and endometrium (HEC-1A) and from a glioma (Hs 683t). NLF-13 were interacted with tumor cells in soft agar or agarose media using 2 experimental protocols. In 1 system, NLF-13 cells were grown as anchored monolayers proliferating under the tumor cell layer. In the 2nd, NLF-13 were embedded directly (nonanchored) into the agar or agarose layer with the tumor cells. The results from both interaction systems were similar for all 5 tumor lines. Anchored NLF-13 caused a dose-dependent inhibition of tumor growth; nonanchored cells produced a dose-dependent growth stimulation. A time exposure experiment indicated that tumor stimulation and inhibition were biphasic responses to NLF-13. Evidently, low concentrations of a diffusible NLF-13 product(s) accelerated tumor growth, while high concentrations were inhibitory. The production of the active NLF-13 substance(s) was positively correlated with NLF-13 growth rate. Tumor cell inhibition was irreversible after a 5 day exposure to proliferating NLF-13 cells. Another line of normal neonatal human lung fibroblasts (NLF-147) showed inhibitory properties similar to those described for NLF-13. Preliminary studies with fibroblasts from the skin of a Down''s syndrome neonate (DS-172) and from a human kidney tumor (KTF-130) have shown both these fibroblast types to have a reduced ability to inhibit tumor cell cultures (J82) compared to the neonatal lung fibroblasts (NLF-13 and NLF-147).