Mitogenic potential of insulin on lymphoma cells lacking IGF-1 receptor.
We have characterized an insulin-dependent T-cell lymphoma, LB, devoid of IGF-I receptor, which undergoes insulin stimulation and cell proliferation both in vitro and in vivo. In these cells, the mitogenic response can be evoked only through binding of insulin to its own receptor. This lymphoma is thus a good model for studying the molecular mechanisms involved in insulin mitogenicity. The high level of activated Ras in LB cells, even under nonproliferative conditions, shows that activation of Ras is insufficient for mitogenicity. It has been suggested earlier that separate pathways of signal transduction may emerge from Ras. The decision to activate a certain signaling pathway may depend on the activation state of other signaling routes in the cell. This may be the case in LB cells, where a signaling component activated by insulin works in concert with the Ras signaling pathway to induce mitogenesis. Yet it is still unclear whether activated Ras is a prerequisite for the insulin-induced response in LB cells.
D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D006801:Humans; D007328:Insulin / Q000494:pharmacology*; D007700:Kinetics; D016399:Lymphoma, T-Cell / Q000473:pathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008934:Mitogens / Q000494:pharmacology*; D017526:Receptor, IGF Type 1 / Q000235:genetics / Q000502:physiology*; D011972:Receptor, Insulin / Q000276:immunology / Q000502:physiology*; D015398:Signal Transduction; D014407:Tumor Cells, Cultured
D000906:Antibodies; D007328:Insulin; D008934:Mitogens; D017526:Receptor, IGF Type 1; D011972:Receptor, Insulin