Objective: To investigate the possible relationship between liver-specific insulin-like growth factor I (IGF-1) and the pathogenesis of breast cancer.
Methods: Fifty non-IGF-1 deficient (LID) mice were randomly divided into 2 equal groups: Group I, fed with dimethyl-benzanthracene (DMBA) for 8 weeks to cause mammary cancer, and Group III, fed with DMBA and ginsenoside Rg for 28 d; and 50 LID mice were randomly divided into 2 equal groups too Group II, fed with DMBA for 8 weeks, and Group IV, fed with DMBA and ginsenoside Rg for 28 d. The mice were killed after the cessation of DMBA use. The serum IGF-1 expression was detected with method Six Gene chips were used to detect the gene expression in the breast cancer tissues.
Results: The breast cancer rates were 66.67% in Group I and 33.33% in Group II, 36.00% in Group III, and 12.00% in Group IV. The tumor size was (0.79 +/- 0.20) cm in Group I, (0.37 +/- 0.08) cm in Group III , (0.32 +/- 0.08) cm in Group II, and (0.15 +/- 0.05) cm Group IV. The IGF-1 level of Group II was (41.33 +/- 7.52) ng/ml, 1/4 as high as that of Group I [(166.51 +/- 12.32) ng/ml], and the IGF-1 level of Group IV was (33.48 +/- 6.73) ng/ml, 1/4 as high as that of Group III [(155.84 +/- 11.34) ng/ml]. Compared with those of the control mice, the breast cancers of the LID mice had longer latency, lower incidence, and slower growth rate. The differential gene expression in different serum IGF-1 levels involved binding, metabolism, apoptosis, cell cycle, signal transduction, immune response, transcription regulation and interpretation regulation and so on. Among these genes, Col11, Egln3, Glycam1, Irf6, Lgals7, Perp, Rag1, and Rbm35a genes were closely related to the incidence of breast cancer.
Conclusion: IGF-1 plays a role as a risk factor in the onset and development of breast cancer by affecting the expression of many differentially expressed genes.