Selective reduction in receptors for epidermal growth factor-urogastrone in chemically transformed tumorigenic Syrian hamster embryo fibroblasts.

Receptors for insulin and epidermal growth factor-urogastrone (EGF-URO) have been measured in Syrian hamster em bryo fibroblasts and in a benzo(a)pyrene-transformed tumorigenie cell line (BP6T). Compared with the parent Syrian ham ster embryo cells, the BP6T cells exhibit a marked reduction in the binding of EGF-URO, whereas the binding of insulin is the same in both cell types. The selective reduction in EGF-URO receptors in BP6T cells cannot be attributed to changes in receptor-binding kinetics, to the presence in BP6T cultures of either receptor blockingor receptor-destroying activities, to differences in EGF-URO degradation, to effects of cell density on receptor numbers, or to a glycosylation defect that can be corrected by supplementing cells with /V-acetylglucosamine. It is suggested that changes either in receptor turnover rates or in receptor characteristics apart from ligand recognition may account for reduced receptor availability in the transformed cells. Like BP6T cells, other chemically transformed tumorigenie cell lines derived from Syrian hamster embryo cells also exhibit reduced EGF-URO binding compared with the parent Syrian hamster embryo cell strain. However, the amount of binding of EGF-URO by transformed cells does not correlate either with the cellular growth characteristics (generation time and cloning efficiency in agar) or with the ability of cells to cause tumors in vivo. Thus, while the selective reduction in EGF-URO receptors may be a feature of cell transformation, a direct relationship between this receptor reduction and cellular tumorigenesis appears to be nonexistent.