Simian virus 40 large tumor antigen is unable to transform mouse embryonic fibroblasts lacking type 1 insulin-like growth factor receptor.

摘要: Abstract Fibroblast cell lines were established from mouse embryos homozygous for a targeted disruption of the Igf1r gene, encoding type 1 receptor insulin-like growth factor I (IGF-I) and their wild-type littermates. The cells (W cells) grow in serum-free medium supplemented with platelet-derived factor, epidermal IGF-I, whereas Igf1r(-/-) (R- do not, although they at reduced rate 10% fetal calf serum. simian virus 40 (SV40) large T antigen, expressed transfected plasmid, can transform W cells, which form foci monolayer cultures colonies soft agar (anchorage-independent growth). In contrast, SV40 tumor normally template, is unable to R- remain contact-inhibited fail agar. transformed phenotype restored if carrying antigen are stably plasmid expressing human IGF-I receptor. These results demonstrate that signaling via an indispensable component transformation pathway. This conclusion further supported antisense RNA experiments showing interference function has profound effect on anchorage-independent growth, even under conditions only modestly affect monolayers.