Conclusions
IGF-1R is overexpressed in breast cancer tissues. The overexpressed IGF-1R promotes the expression of cyclin D1 protein and accelerates the G1/S transition by activating Ras/Raf/MEK/ERK signaling pathway, thus further promoting cell proliferation and the carcinogenesis of breast cancer.
Methods
The expression of IGF-1R protein in breast cancer tissues and the adjacent normal tissues was detected by immunohistochemistry. By IGF-1R inhibitor mediated repression of IGF-1R expression in MCF-7 cells, the cell proliferation rate, cell cycle and the expression of Ras/Raf/MEK/ERK signaling pathway proteins as well as cyclin D1 protein were examined in the IGF-1R-inhibited cells.
Objective
The objective of study was to detect the expression level of IGF-1R in breast cancer tissues and investigate the effect of IGF-1R expression on the proliferation and apoptosis of breast cancer cells.
Results
The proportion of IGF-1R, cyclin D1, Ras and p-ERK1/2 positive cells in breast cancer tissues were (69.8±12.7)%, (38.0±6.2)%, (71.6±10.3)% and (3.1±5.7)%, respectively, which were all significantly higher than those in the adjacent normal tissues [(16.2±6.7)%, (0.5±0.7)%, (7.1±0.9)% and (12.2±5.4)%] (P<0.05). Compared to normal MCF-7 cells, the MCF-7 cells treated with IGF-1R inhibitor showed no expression of IGF-1R protein, increased apoptosis rate (370.3%), increased proportion of cells in G1 phase (81.1%), decreased proportion of cells in S phase (66.8%), decreased proportion of cells in G2/M phase (52.9%), decreased Ras protein expression (70.9%), decreased p-ERK1/2 protein expression (53.3%), decreased cyclin D1 protein expression (59.5%), and substantially unchanged expression of ERK1/2 protein (P<0.05). Conclusions: IGF-1R is overexpressed in breast cancer tissues. The overexpressed IGF-1R promotes the expression of cyclin D1 protein and accelerates the G1/S transition by activating Ras/Raf/MEK/ERK signaling pathway, thus further promoting cell proliferation and the carcinogenesis of breast cancer.