Chitooligosaccharides induce apoptosis in human breast cancer cells

Abstract

In this study, biologically active chitooligosaccharides (COS) D3–7 (D-deacetylated unit) and A5 (A-acetylated unit) were assessed for their suitability to reduce the viability of human breast cancer cell lines, BT-474 and SUM-159. The treatment with COS resulted in a significant decrease in the viability of breast cancer cells, in a dose-dependent manner. The long-term proliferative potential of breast cancer cells decreased upon COS treatment, suggesting that COS significantly inhibited colony formation in breast cancer cells. The COS-treated cell population significantly underwent apoptosis, confirmed by flow cytometry. Further, the increased expression of BAX, cleaved PARP, and cleaved caspase 3, with increased concentration of COS, conformed that COS-D3–7 and A5 induce apoptosis in BT474 cells through apoptotic signaling. We further investigated the mechanism by which COS promotes apoptosis. The marked inhibition of phosphorylation of EGFR and its downstream signaling molecules FAK, AKT, and MAPKpromote apoptosis.