Abstract

The objective of this study is to examine the impact of caffeic acid on triple negative breast cancer by regulating epidermal growth factor receptor/signal transduction and activator of transcription 3/protein kinase B pathway related proteins. The blank control group cells were immortalized human normal breast epithelial cell line MCF-10A, without any treatment, and were cultured routinely; the cells in the triple negative breast cancer group were human triple negative breast cancer MDA-MB-231 cells, which were routinely cultured without any treatment; in caffeic acid p-nitrophenyl ethyl ester group, human triple negative breast cancer MDA-MB-231 cells were added with caffeic acid p-nitrophenyl ethyl ester 10 μg/ml. After continue to incubate in the incubator for 48 h. The proliferation activity and the number of cell migration of caffeic acid on nitrophenylethyl ester group were lower compared to the triple negative breast cancer group. The number of cell invasion of caffeic acid on nitrophenylethyl ester group was lower in comparison to the triple negative breast cancer group, and the apoptosis rate exhibited a statistically significant increase in comparison to the triple negative breast cancer group. The levels of epidermal growth factor receptor, signal transduction and activator of transcription 3, protein kinase B, messenger ribonucleic acid, and protein were found to be significantly lower in the caffeic acid group compared to the triple negative breast cancer group. The expression levels of matrix metalloproteinase-2, matrix metalloproteinase-9 and vascular endothelial growth factor-A protein in the caffeic acid nitrophenethyl group were lower in comparison to the triple negative breast cancer group. Caffeic acid p-nitrophenyl ethyl ester can reduce the activity of triple negative breast cancer cells, inhibit the growth, migration and invasion of triple negative breast cancer cells, and induce apoptosis of colorectal cancer cells. The mechanism potentially exhibits a correlation with the regulation of the epidermal growth factor receptor/signal transduction and activator of transcription 3/protein kinase B signaling pathway.