Objective: A stable primary breast cancer model in liver-specific insulin-like growth factor 1 (IGF-1) deficient (LID) mice and control mice was established. To screen apoptosis related genes expression in different serum IGF-1 levels by gene chip and flow cytometry.
Methods: The LID mice and control mice were used. Induction of breast cancer was achieved by using the 7,12-dimethylbenz(a) anthracene. Ginsenoside Rg3 was used to interfering therapy treatment. The incidence of breast cancer in every group was compared, and expression of apoptosis associated genes was detected by gene chip and flow cytometry.
Results: The incidence of tumor in none ginsenoside Rg3 injected control mice was 66.7%. The incidence of tumor in ginsenoside Rg3 injected LID mice was 12.0% which was significantly lower than any other group (P < 0.05). The apoptosis percentage in none ginsenoside Rg3 injected control mice was (2.7 +/- 0.7)%. The apoptosis percentage in ginsenoside Rg3 injected LID mice was (14.0 +/- 1.7)%. The results of gene chip indicated that in contrast to LID mice, LTA, LTB, TNF-alpha, TRAIL, TRANCE, BLK, BOK, CASP8, TRAF5, and APAF1 genes were down-regulated, and LTBR, TRAF4 genes were up-regulated in the breast cancer tissues of control mice. Application of ginsenoside Rg3 therapy could change the expression of these genes.
Conclusions: Circulating IGF-1 levels play a role in the onset and development of breast cancer. Degrade serum IGF-1 level is able to promote apoptosis by affecting the expression of a series of apoptosis related genes consequently inhibit the growth of breast cancer. There was a synergistic effect with the application of ginsenoside Rg3.